Molecular And Cellular Probes[JOURNAL]
Sun
200 papers
MicroRNA-130 as a critical modulator of cardiac remodeling: interplay between autophagic flux and ferroptotic pathways in acute myocardial infarction.
Chen L, Jiang D, Kou W … +1 more , Xu Y
Mol Cell Probes · 2025 Oct · PMID 40523509 · Publisher ↗
BACKGROUND: Acute myocardial infarction (AMI) continues to be a leading cause of morbidity and death. OBJECTIVE: This study investigates miR-130's regulatory mechanisms in AMI progression. METHODS: Bioinformatics analysi...
BACKGROUND: Acute myocardial infarction (AMI) continues to be a leading cause of morbidity and death. OBJECTIVE: This study investigates miR-130's regulatory mechanisms in AMI progression. METHODS: Bioinformatics analysis of miR-130 conservation and differential expression was performed using miRbase and Gene Expression Omnibus datasets. Angiotensin II (Ang II)-treated H9C2 cardiomyocytes modeled AMI in vitro. miR-130 inhibitor/mimic transfection, combined with autophagy inhibitor Spautin-1 or ferroptosis inhibitor Ferrostatin-1, were assessed via qPCR, ELISA (PC III, HA, CTnT, CK-MB), Western blot (LC3-II/LC3-I, p62, SLC7A11, GPX4), and flow cytometry. RESULTS: Our results demonstrate that Ang II stimulation significantly elevates miR-130 expression in H9C2 cells, concomitant with increased secretion of myocardial injury and fibrosis markers. Inhibition of miR-130 markedly improved cell viability and reduced apoptosis, accompanied by decreased expression of fibrosis markers such as α-SMA and Collagen I, and a rebalancing of autophagy dynamics, as indicated by an increased LC3-II/LC3-I ratio and elevated p62 levels. Conversely, miR-130 overexpression via a synthetic mimic reduced cell viability and enhanced apoptosis, with a corresponding rise in fibrosis markers (PC III, HA, CTnT, CK-MB) and disruption of both autophagy and ferroptosis pathways, evidenced by decreased levels of SLC7A11 and GPX4. Notably, the adverse effects induced by miR-130 mimic were effectively reversed by Spautin-1 and Ferrostatin-1 co-treatment, suggesting that miR-130 modulates AMI-related cellular responses through intertwined autophagy and ferroptosis mechanisms. CONCLUSION: These findings reveal that miR-130 is a pivotal regulator of myocardial injury in AMI, mediating its effects via the modulation of autophagy and ferroptosis pathways. Targeting miR-130 may therefore represent a promising therapeutic strategy for mitigating myocardial damage and improving cardiac function following AMI.
DNMT3A triggers tumorigenesis of non-small cell lung cancer through regulation of SLIT2 methylation and SLIT2-mediated macrophage M1/M2 polarization.
Ni TX, Shen JB
Mol Cell Probes · 2025 Aug · PMID 40447165 · Publisher ↗
BACKGROUND: Increased DNA methylation is prevalent in human cancers and is one of the important characteristics of tumors. This research aims to investigate the molecular mechanisms that involve DNMT3A and DNA methylatio...
BACKGROUND: Increased DNA methylation is prevalent in human cancers and is one of the important characteristics of tumors. This research aims to investigate the molecular mechanisms that involve DNMT3A and DNA methylation modification of SLIT2 in non-small cell lung cancer (NSCLC). METHODS: Gene expression was examined using Western blot assay, immunohistochemistry and RT-qPCR. Cell viability and motility were measured by CCK-8, colony formation, Transwell and wound healing assays. Macrophage M1/M2 polarization was assessed through a flow cytometry assay. Using ELISA, the secretion levels of inflammatory factors by macrophage M1/M2 polarization were determined. ChIP, qMSP and dual-luciferase reporter assays confirmed the relationship between DNMT3A and SLIT2. RESULTS: High expression of DNMT3A was observed in NSCLC patients, enhancing NSCLC cell viability and metastasis. Mechanically, DNMT3A was identified to target SLIT2. DNMT3A inhibited SLIT2 expression through DNA methylation modification in NSCLC. Further, overexpression of SLIT2 impeded M2 polarization of macrophages in NSCLC. And SLIT2 overexpression hindered NSCLC tumor growth in vivo by affecting macrophage M2 polarization. Finally, DNMT3A was found to promote the progression of NSCLC by downregulating SLIT2. CONCLUSION: DNMT3A promotes the progression of NSCLC via regulating methylation modification of SLIT2 and SLIT2-mediated macrophage M1/M2 polarization.
Gastrodin promotes osteogenic differentiation by stimulating the Wnt/β-catenin signaling pathway.
Jiang W, Zhang L, Shan W … +3 more , Wu Z, Wang J, Shen C
Mol Cell Probes · 2025 Aug · PMID 40436074 · Publisher ↗
BACKGROUND: Osteoporosis is a common disease that can lead to fracture as well as various skeletal symptoms and is a global health problem. Traditional Chinese medicine (TCM) may offer novel approaches for treating osteo...
BACKGROUND: Osteoporosis is a common disease that can lead to fracture as well as various skeletal symptoms and is a global health problem. Traditional Chinese medicine (TCM) may offer novel approaches for treating osteoporosis. Our study aimed to investigate the osteogenic potential and underlying mechanisms of gastrodin in promoting osteogenic differentiation. METHODS: By combining network pharmacology and bioinformatics, we conducted experiments to inspect cell viability, Alkaline Phosphatase (ALP) viability, and Alizarin red staining (ARS) and investigate the expression profiles of genes and proteins relevant to osteogenesis, including β-catenin, Runt-related transcription factor 2 (Runx2), Low Density Lipoprotein Receptor-Related Protein 5 (LRP5) and Glycogen synthase kinase-3 beta (GSK-3β). Statistical analysis was used for validation. RESULTS: Network pharmacology and bioinformatics analyses revealed that gastrodin might influence osteogenic differentiation. The experimental results revealed that gastrodin had no toxic effects and was able to promote ALP activity and stimulate osteogenic differentiation of Mouse Calvaria-derived Osteoblastic Cell Line. (MC3T3-E1) cells. Subsequent network pharmacology and bioinformatics studies revealed that gastrodin might affect osteogenic differentiation through the Wnt/β-catenin signaling pathway. The results revealed that gastrodin influenced osteogenic differentiation genes and protein expression, including the upregulation of β-catenin, Runx2, and LRP5 and the downregulation of GSK-3β, and Dickkopf-1 (DKK-1) inhibited its promotion. CONCLUSION: Gastrodin enhances the Wingless (Wnt)/β-catenin signaling pathway by increasing β-catenin accumulation and nuclear migration as well as decreasing GSK-3β, which increases Runx2 expression, consequently encouraging MC3T3-E1 cell osteogenic differentiation, and may be applied as a potential drug for osteoporosis therapy and prevention.
Transcriptional regulation of tumor suppressor gene RASSF1A by HBx.
Kang Y, Li W, Wei J … +2 more , Yang L, Kang Y
Mol Cell Probes · 2025 Aug · PMID 40419121 · Publisher ↗
INTRODUCTION: The occurrence of liver cancer in China is primarily attributed to chronic hepatitis B virus (HBV) infection. HBV X protein (HBx) has emerged as a significant carcinogenic driver in HBV-related liver cancer...
INTRODUCTION: The occurrence of liver cancer in China is primarily attributed to chronic hepatitis B virus (HBV) infection. HBV X protein (HBx) has emerged as a significant carcinogenic driver in HBV-related liver cancer. However, the underlying mechanism by which HBx contributes to liver cancer development is not fully understood. METHODS: This study investigated HBx's role in regulating the tumor-suppressor gene RASSF1A. Firstly, the RASSF1A plasmid was constructed using a luciferase reporter system. The dual luciferase assay system detected HBx's effect on RASSF1A promoter activity. Western blotting and quantitative PCR methods measured HBx's impact on RASSF1A protein and mRNA expression. Chip was used to test the binding of HBx and SP1. CCK8, transwell, flow cytometry were used to detect the effect of RASSF1A on HCC proliferation. Methylation-specific PCR analyzed HBx's effect on RASSF1A methylation. RESULTS: Our results show that HBx significantly enhances RASSF1A promoter activity in an SP1 binding site-dependent manner. When only one SP1 binding site remained, HBx's effect was abolished. RASSF1A can inhibit HCC proliferation. Both mRNA and protein expression levels of RASSF1A were lower in HBx-expressing THLE-2 cells than in control cells, correlating with higher RASSF1A promoter methylation. CONCLUSION: These findings suggest HBx enhances RASSF1A promoter activity and upregulates transcription via SP1, potentially preceding RASSF1A promoter methylation. This study provides new insights into HBx's regulation of the tumor suppressor gene RASSF1A in HBV-related liver cancer.
Exosomal lncRNA profiles in patients with HFrEF: Evidence for KLF3-AS1 as a novel diagnostic biomarker.
Wang L, Zhang Y, Wang J … +5 more , Jiang X, Wang G, Wang H, Shu Y, Huiyuan H
Mol Cell Probes · 2025 Aug · PMID 40404068 · Publisher ↗
BACKGROUND: Serum exosomal long noncoding RNAs (lncRNAs) have not been studied extensively as biomarkers in heart failure (HF) with reduced ejection fraction (HFrEF). We compared lncRNA expression in patients with HFrEF...
BACKGROUND: Serum exosomal long noncoding RNAs (lncRNAs) have not been studied extensively as biomarkers in heart failure (HF) with reduced ejection fraction (HFrEF). We compared lncRNA expression in patients with HFrEF hospitalized for acute HF with that in healthy individuals to identify differentially expressed exosomal lncRNAs. Furthermore, we explored the clinical value of exosomal KLF3-AS1 in diagnosing HF and investigated its role in cardiac hypertrophy. METHOD: Exosomes were isolated from patients with HFrEF and healthy individuals. We performed microarray analysis of differentially expressed lncRNAs and genes (DELs and DEGs, respectively) associated with HF. Protein-protein interaction (PPI), lncRNA-mRNA-KEGG pathway, and interaction networks between lncRNAs and RNA-binding proteins (RBPs) were developed. Expression patterns were verified using qRT-PCR. The diagnostic applicability of exosomal lncRNAs in HF was quantified by plotting receiver operating characteristic (ROC) curves. The size of the cardiomyocytes was evaluated using α-actinin immunostaining. RESULTS: In total, 138 DELs and 1132 DEGs were identified. PPI network analysis identified INS, CTNNB1, and CAT as the most prominent hub genes, whereas MDM2, MYH6, ENAH, and KLF3-AS1 were significantly enriched in the RBP interaction network. In the validation phase, patients with HFrEF exhibited a significant increase in KLF3-AS1 expression compared with healthy individuals. Exosomal KLF3-AS1 had an area under the ROC curve of 0.861. Functionally, KLF3-AS1 overexpression reduced Ang II-induced cardiac hypertrophy in vitro. CONCLUSION: Our results elucidated the exact patterns of circulating exosomal mRNAs and lncRNA expression in patients with HFrEF hospitalized for acute HF. Moreover, the high expression of exosomal KLF3-AS1 is a potential diagnostic biomarker for HFrEF.
Screening and identification Hub genes associated with immune cell infiltration and critical biomarkers in osteosarcoma.
Song X, Chen S, Cheng J … +7 more , Li H, Wu R, Yan M, Wang M, Li J, Jin A, Wang W
Mol Cell Probes · 2025 Aug · PMID 40374042 · Publisher ↗
PURPOSE: Osteosarcoma (OS) exhibits limited immune cell infiltration that directly contributes to poor prognosis. This study sought to screen and identify pivotal biomarkers of OS immune infiltration and early diagnosis...
PURPOSE: Osteosarcoma (OS) exhibits limited immune cell infiltration that directly contributes to poor prognosis. This study sought to screen and identify pivotal biomarkers of OS immune infiltration and early diagnosis of OS. METHODS: The immune cell infiltration profiles with transcriptome sequencing data from 88 OS samples were explored with CIBERSORT algorithm. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) and Protein-protein interaction (PPI) network analyses were applied to identify hub genes, with the expressions confirmed by dual immunofluorescence in 50 OS samples. The new biomarker gene HTRA1 were examined by immunohistochemistry and validated by the Immune score and immune gene expression profile analyses. The impact of HTRA1 on OS prognosis was verified by Least absolute shrinkage and selection operator (LASSO) regression analysis. The biological effect of HTRA1 was characterized in MG63 cells. RESULT: CD8 T cells, activated memory CD4 T cells and plasma cells were positively correlated with the prognosis of OS. Hub genes CCL5, CXCL9, CXCL13, and HTRA1, exhibited positive correlation with the infiltration of both CD8 T cells and CD4 T cells. HTRA1 expression was reduced in osteosarcoma tissues, which was positively correlated with immune scores and the expressions of immune-related genes. High levels of HTRA1 were associated with favorable OS prognosis, and could negatively impacted MG63 malignant characteristics. CONCLUSION: CCL5, CXCL9, CXCL13, and HTRA1 were OS hub genes positively correlate with CD8 T cell and CD4 T cell infiltrations. HTRA1 can serve as an underlying biomarker for the prognosis and immunotherapy of OS.
ANP32E expression in pancreatic cancer is associated with impaired gemcitabine efficacy and poor patient prognosis.
Liu X, Zhao Y, Zhang L … +15 more , Wang J, Luo L, Zhang S, Zhu Q, Shi Y, Yuan C, Xiao Q, Xiong M, Duan Y, Chen H, Yao H, Cai L, Zhang J, Li G, Li L
Mol Cell Probes · 2025 Aug · PMID 40306467 · Publisher ↗
PURPOSE: Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive and fatal malignancy, although gemcitabine is administered as a single or combined therapeutic agent. Our previous study demonstrated that ANP32E ov...
PURPOSE: Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive and fatal malignancy, although gemcitabine is administered as a single or combined therapeutic agent. Our previous study demonstrated that ANP32E overexpression promoted PDAC cell proliferation. However, whether it affects treatment outcome and clinical prognosis is still unclear. In the present study, we aimed to determine whether ANP32E is negatively associated with the treatment outcome of gemcitabine. METHODS: We collected clinical characteristics and treatment information from a total of 75 PDAC patients to assess the association of ANP32E expression via immunohistochemical (IHC) staining with overall survival (OS) in patients who were or were not treated with gemcitabine-based chemotherapy, followed by a clinical replication study with transcriptomic data from the TCGA database and functional validation experiments involving the knockdown of ANP32E in the Hup-T3 and SU86.86 human pancreatic cancer cell lines. RESULTS: We demonstrated the interference effect of ANP32E on gemcitabine efficacy and patient prognosis in PDAC patients by using our own clinical samples or publicly available TCGA datasets. Downregulation of ANP32E significantly sensitized Hup-T3 and SU86.86 cells to gemcitabine, which was consistent with the results of the above association studies. CONCLUSION: Our findings suggest that ANP32E might serve as a negative biomarker for poor prognosis and a predictive indicator for poor gemcitabine efficacy. These findings suggest that ANP32E might be a potential therapeutic target to help develop effective drugs to overcome gemcitabine resistance and reduce the risk for relapse or metastasis in patients with PDAC.
The clinicopathologic and prognostic value of CD44 expression in patients with non-small cell lung cancer: A systematic review and meta-analysis.
Alaei E, Farahani N, Orouei S … +7 more , Alimohammadi M, Daneshi S, Mousavi T, Mahmoodieh B, Taheriazam A, Rahimzadeh P, Hashemi M
Mol Cell Probes · 2025 Jun · PMID 40139282 · Publisher ↗
BACKGROUND: CD44 is a promising target in the prognosis and treatment of non-small cell lung cancer (NSCLC). The study deals with systematic review and meta-analysis to determine the association between CD44 overexpressi...
BACKGROUND: CD44 is a promising target in the prognosis and treatment of non-small cell lung cancer (NSCLC). The study deals with systematic review and meta-analysis to determine the association between CD44 overexpression and survival and clinicopathological characteristics in NSCLC patients. METHODS: We used the databases Google Scholar, Web of Science, PubMed, Scopus, EMBASE, and Cochrane to conduct a systematic search of English-language literature published up to September 2023. The eligible studies were retrieved on CD44 expression, clinicopathological characteristics in NSCLC patients, and reported survival rates. The Cochran's and Higgins I tests were used to measure heterogeneity across the included studies. P < 0.05 was considered statistically significant in all cases. The sources of heterogeneity across the included studies were identified using subgroup analysis on histology (SCC, ADC, and LCC), tumor differentiation (well, moderate, and poor), TMN stage (I/II/III/IV), OS, and lymph node metastasis (negative and positive). All statistical analyses were carried out using meta-analysis (CMA) software. RESULTS: The final analysis for prognostic significance and clinicopathological features on 3681 participants from 25 eligible studies. The pooled event rate of overexpression CD44 for overall survival in NSCLC was 38 % and was related to SCC with 76.6 %. Furthermore, subgroup analysis revealed a link between CD44 overexpression and moderate tumor differentiation (41.8 %). There was a substantial difference in CD44 overexpression in males, with 69.3 % (95 % CI: 64.3-73.9 %, I = 88.25 %) versus 31.5 % (95 % CI: 26.7-36.8 %, I = 92.15 %) in females. However, no significant relationship was observed between CD44 overexpression and TMN stages/lymph node metastasis. CONCLUSION: The meta-analysis demonstrated that CD44 is an effective prognostic factor for NSCLC. Overexpression of CD44 has been linked to moderate tumor differentiation, SCC tumor histology, and a worse survival rate. However, no substantial relationship was found between CD44 and metastasis or TMN stages. Large-scale prospective research is required to validate CD44's clinical value as an unbiased prognostic indicator.
Transcriptomic analysis of intracellular RNA granules and small extracellular vesicles: Unmasking their overlap in a cell model of Huntington's disease.
Nabariya DK, Knüpfer LM, Hartwich P … +3 more , Killian MS, Centler F, Krauß S
Mol Cell Probes · 2025 Jun · PMID 40090627 · Publisher ↗
Huntington's disease (HD) arises from the abnormal expansion of a CAG repeat in the HTT gene. The mutant CAG repeat triggers aberrant RNA-protein interactions and translates into toxic aggregate-prone polyglutamine prote...
Huntington's disease (HD) arises from the abnormal expansion of a CAG repeat in the HTT gene. The mutant CAG repeat triggers aberrant RNA-protein interactions and translates into toxic aggregate-prone polyglutamine protein. These aberrant RNA-protein ineractions also seed the formation of cytoplasmic liquid-like granules, such as stress granules. Emerging evidence demonstrates that granules formed via liquid-liquid phase separation can mature into gel-like inclusions that persist within the cell and may act as precursor to aggregates that occur in patients' tissue. Thus, deregulation of RNA granules is an important component of neurodegeneration. Interestingly, both the formation of intracellular membrane-less organelles like stress granules and the secretion of small extracellular vesicles (sEVs) increase upon stress and under disease conditions. sEVs are lipid membrane-bound particles that are secreted from all cell types and may participate in the spreading of misfolded proteins and aberrant RNA-protein complexes across the central nervous system in neurodegenerative diseases like HD. In this study, we performed a comparative transcriptomic analysis of sEVs and RNA granules in an HD model. RNA granules and sEVs were isolated from an inducible HD cell model. Both sEVs and RNA granules were isolated from induced (HD) and non-induced (control) cells and analyzed by RNA sequencing. Our comparative analysis between the transcriptomics data of HD RNA granules and sEVs showed that: (I) intracellular RNA granules and extracellular RNA vesicles share content, (II) several non-coding RNAs translocate to RNA granules, and (III) the composition of RNA granules and sEVs is affected in HD cells. Our data showing common transcripts in intracellular RNA granules and extracellular sEVs suggest that formation of RNA granules and sEV loading may be related. Moreover, we found a high abundance of lncRNAs in both control and HD samples, with several transcripts under REST regulation, highlighting their potential role in HD pathogenesis and selective incorporation into sEVs. The transcriptome cargo of RNA granules or sEVs may serve as a source for diagnostic strategies. For example, disease-specific RNA-signatures of sEVs can serve as biomarker of central nervous system diseases. Therefore, we compared our dataset to transcriptomic data from HD patient sEVs in blood. However, our data suggest that the cell-type specific signature of sEV-secreted RNAs as well as their high variability may make it difficult to detect these biomarkers in blood.
Differential gene expression in uterine endometrioid cancer cells and adjusted normal tissue.
Kodada D, Hadžega D, Krumpolec P … +7 more , Janoštiaková N, Bľandová G, Janega P, Ballová Z, Dosedla E, Minárik G, Repiská V
Mol Cell Probes · 2025 Jun · PMID 40090626 · Publisher ↗
Endometrial cancer is a significant public health concern with rising incidence rates globally. Understanding the molecular mechanisms underlying this disease is crucial for developing effective therapeutic strategies. O...
Endometrial cancer is a significant public health concern with rising incidence rates globally. Understanding the molecular mechanisms underlying this disease is crucial for developing effective therapeutic strategies. Our study aimed to characterize transcriptional changes in endometrial cancer tissues compared to adjusted healthy tissue. Using RNA sequencing, we identified 2483 differentially expressed genes (DEGs), including protein-coding genes, long non-coding RNAs (lncRNAs), and microRNAs (miRNAs). Notably, several known cancer-related genes were differentially expressed, such as MYC, AKT3, CCND1, and CDKN2A. Pathway analysis revealed significant alterations in cell cycle regulation, several signaling pathways, and metabolic processes. These findings provide valuable insights into the molecular pathways dysregulated in endometrial cancer. Our results may contribute to the development of novel therapeutic targets and biomarkers for this disease.
BUB1-deficiency suppresses kidney renal clear cell carcinoma progression via the PI3K/Akt pathway: A bioinformatics-oriented validating study.
Zi X, Ma J, Li X … +4 more , Wang H, Bao Y, Deng T, Yuan X
Mol Cell Probes · 2025 Jun · PMID 40081509 · Publisher ↗
Although great advances have been reached in the diagnosis, treatment and prognosis of kidney renal clear cell carcinoma (KIRC), the advancement of therapeutic strategies for KIRC in clinical practices have been seriousl...
Although great advances have been reached in the diagnosis, treatment and prognosis of kidney renal clear cell carcinoma (KIRC), the advancement of therapeutic strategies for KIRC in clinical practices have been seriously limited due to its unknown molecular mechanisms. To resolve this issue, through analyzing the datasets from the online UCSC database, a novel BUB1 gene was found to be elevated in the cancerous tissues compared to their normal tissues of KIRC, and and KIRC patients with high-expressed BUB1 tended to have a worse prognosis. The subsequent experiments validated that BUB1 protein was located in both nucleus and cytoplasm of KIRC cells, and the expression levels of BUB1 gene were significantly elevated in KIRC tissues and cells, in contrast to their normal counterparts. Loss-of-function experiments verified that knockdown of BUB1 suppressed cell proliferation, mobility, epithelial-mesenchymal transition (EMT) and tumor growth, whereas induced apoptotic cell death in the KIRC cells in vitro and in vivo. In addition, bioinformatics analysis predicted that the differentially-expressed genes (DEGs) in the BUB1-deficient cohorts were enriched in the cell division-related PI3K/Akt signal pathway, and we evidenced that silencing of BUB1 was capable of inactivating the downstream PI3K/Akt signal pathway. Of note, deficiency of BUB1-induced suppressing effects on the malignant phenotypes in KIRC cells were all reversed by co-treating cells with PI3K/Akt pathway activator 740Y-P. Furthermore, it was found that the expression status of BUB1 gene were related with epigenetic modifications, immune infiltration and immunotherapy responses in KIRC. Collectively, silencing of BUB1 inhibited the progression of KIRC through inactivating the downstream PI3K/Akt signal pathway, and BUB1 gene could be potentially used as biomarkers for the diagnosis and treatment of KIRC in clinic.
Down-regulated circ_0001853 inhibits lipopolysaccharide-induced endometritis progression via sponging miR-34c-5p.
Xu Q, Peng A, Zhao L … +1 more , Wang L
Mol Cell Probes · 2025 Jun · PMID 40058671 · Publisher ↗
BACKGROUND: To investigate the diagnostic value and mechanism of action of circular RNA (circ_) circ_0001853 and microRNA (miR) miR-34c-5p in patients with endometritis. METHODS: 189 patients with endometritis and 176 he...
BACKGROUND: To investigate the diagnostic value and mechanism of action of circular RNA (circ_) circ_0001853 and microRNA (miR) miR-34c-5p in patients with endometritis. METHODS: 189 patients with endometritis and 176 healthy individuals were included in this study. Venous blood serum was collected from the study subjects and stored temporarily at -80 °C. Real-time quantitative chain polymerase reaction (RT-qPCR) was used to detect circ_0001853 and miR-34c-5p expression, and receiver operating characteristic (ROC) curves assessed the diagnostic value of both in predicting endometritis. Cell counting kit (CCK8) observed cell proliferation, flow cytometry recorded apoptosis, enzyme linked immunosorbent assay (ELISA) monitored inflammatory factor expression, and dual luciferase reporter assay and RNA immunoprecipitation (RIP) verified the relationship between circ_0001853 and miR-34c-5p targeting interactions. RESULTS: High levels of circ_0001853 and low levels of miR-34c-5p were present in endometritis patients, and they were negatively correlated. Both circ_0001853 and miR-34c-5p alone or in combination had diagnostic value in predicting the progression of endometritis. Transfection of si-circ_0001853 promoted cell proliferation and reduced apoptosis and cellular inflammation levels induced by lipopolysaccharide (LPS) stimulation. There was a direct reciprocal targeting relationship between miR-34c-5p and circ_0001853, and the use of miR-34c-5p inhibitor resisted silencing circ_0001853 promoted cell proliferation and increased the number of apoptotic cells and cellular inflammation levels. CONCLUSIONS: circ_0001853 is involved in endometritis progression through miR-34c-5p, i.e., low circ_0001853 promotes miR-34c-5p-induced proliferation of epithelial cells, reduces apoptosis, and suppresses inflammation levels, preventing disease progression.
Corrigendum to "Identification of circRNA-mediated competing endogenous RNA network involved in the development of cervical cancer" [Mol. Cell. Probes. 78 (2024) 101984].
Lou S, Yang W, Zhao Q … +3 more , Ouyang Y, Cao L, Lin C
Mol Cell Probes · 2025 Apr · PMID 40057432 · Publisher ↗
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Silymarin plus doxorubicin exerts the anti-hepatocellular carcinoma effects via Wnt, apoptosis, autophagy and angiogenesis pathways.
Yuan B, Wang R, Gao Z … +3 more , Mirzeei H, Xiang AD, Guo F
Mol Cell Probes · 2025 Jun · PMID 40049299 · Publisher ↗
BACKGROUND: The biggest cause of death worldwide is liver cancer. Despite several initiatives and successes in treatment techniques, only a little improvement has been attained. In order to control this cancer, new thera...
BACKGROUND: The biggest cause of death worldwide is liver cancer. Despite several initiatives and successes in treatment techniques, only a little improvement has been attained. In order to control this cancer, new therapeutic strategies are therefore required. Here, we evaluated the effects of doxorubicin and the milk thistle plant phytochemical Silymarin on liver cancer through apoptosis, autophagy, and Wnt signaling. METHODS: Silymarin both alone and together with doxorubicin was administered to induce cytotoxicity in the H22 cell line. qRT-PCR and Western blot analyses, the genes related to autophagy, Wnt signals, and cell death were examined. RESULTS: Doxorubicin and Silymarin both individually and combined dramatically slowed down H22 cells growth. Additionally, there was a significant drop in the Bcl-2 protein and a considerable rise in the caspase 8 and Bax proteins. LC3-I, LC3-II, and Beclin 1 have been all shown to be significantly elevated. Moreover, there was a substantial decrease in the expression of genes involved in the Wnt pathway, including cyclin D1, β-catenin, ZEB1, and Twist. The levels of AMPK were decreased in Silymarin with Doxorubicin alone and in combination, whereas VASP, VEGF, and HIF-1a were lowest. CONCLUSION: Silymarin may enhance anti-tumor effects of doxorubicin through modulating autophagy, angiogenesis, and apoptosis, in-vitro.
Clinical value of microRNA-4449 of non-small cell lung cancer patients undergoing thoracic paravertebral block thoracotomy.
Sun Y, Zhang J, Zhang L … +2 more , Qiu L, Zhang H
Mol Cell Probes · 2025 Apr · PMID 39984060 · Publisher ↗
OBJECTIVE: The aim of this study was to investigate the clinical significance of microRNA-4449 (miR-4449) in patients attacked by non-small cell lung cancer (NSCLC) undergoing thoracic paravertebral block (TPVB) thoracot...
OBJECTIVE: The aim of this study was to investigate the clinical significance of microRNA-4449 (miR-4449) in patients attacked by non-small cell lung cancer (NSCLC) undergoing thoracic paravertebral block (TPVB) thoracotomy. METHODS: A total of 122 patients diagnosed with NSCLC and 101 healthy individuals were recruited in this case-control study. Quantitative real-time polymerase reaction time (qRT-PCR) assay was applied to quantify the serum levels of miR-4449 in all participants. To assess the diagnostic potential of miR-4449, receiver operating characteristic (ROC) curves were constructed. Additionally, the prognostic value of miR-4449 was evaluated using Kaplan-Meier method and Cox regression analyses. The possible target genes and related proteins of miR-4449 were predicted via bioinformatics analysis. RESULTS: MiR-4449 expression was notably reduced in NSCLC patients relative to healthy volunteers (P < 0.001), with the area under the curve (AUC) reaching 0.952, demonstrating its ability to effectively differentiate between NSCLC patients and healthy individuals. Serum levels of miR-4449 were negatively in relation to tumor node metastasis stage and lymph node metastasis (P < 0.05). Moreover, a significant increase in miR-4449 expression was observed in patients following TPVB thoracotomy, as compared to pre-operative levels (P < 0.001). The AUC of 0.884 further highlighted its potential to distinguish between the effective group and the invalid group. Notably, patients expressing high levels of miR-4449 exhibited improved overall survival (P < 0.001), and miR-4449 (P < 0.001, HR = 2.290, 95 % = 1.450-3.615) was identified as an independently prognostic predictor for NSCLC. Bioinformatics analysis of miR-4999 target genes revealed key tumor-associated pathways and proteins, offering valuable insights into its molecular mechanisms in NSCLC. CONCLUSION: Serum levels of miR-4449 were significantly decreased in patients with NSCLC and exhibited a correlation with the severity of the tumor. Furthermore, miR-4449 emerged as a potential prognostic biomarker, offering valuable insight into the clinical outcome for NSCLC undergoing TPVB thoracotomy.
Serum exosomal miR-454-3p contributes to malignant progression of lung cancer by inhibiting HHEX.
Hu G, Cai P, Li J … +3 more , Yu L, Zhao B, Chen G
Mol Cell Probes · 2025 Apr · PMID 39929349 · Publisher ↗
BACKGROUND: Lung cancer is a common cancer. Exosomes are emerging mediators of intercellular communication, and miRNAs serve a crucial position in cancer progression. This project intends to discover whether exosomal miR...
BACKGROUND: Lung cancer is a common cancer. Exosomes are emerging mediators of intercellular communication, and miRNAs serve a crucial position in cancer progression. This project intends to discover whether exosomal miR-454-3p affects tumor progression and its underlying mechanisms. METHODS: Exosomes were isolated utilizing ultracentrifugation. The exosomal biomarkers level was monitored by western blot (WB). The miR-454-3p levels were assessed by quantitative reverse transcription polymerase chain reaction (qRT-PCR), and HHEX expression were detected by qRT-PCR and WB. Cell growth and metastasis were detected through CCK-8, colony formation assay and transwell. Meanwhile, the dual luciferase reporter system and immunoprecipitation (RIP) assay was applied to clarify the interactions between miR-454-3p and HHEX. RESULTS: We successfully isolated serum exosomes from NSCLC patients. Then, our team discovered that miR-454-3p was elevated in serum-derived exosomes from NSCLC patients. Functional analysis disclosed that exosomes accelerated NSCLC cell proliferation and metastasis. Silencing of exosomal miR-454-3p hindered NSCLC cell proliferation and metastasis. Subsequently, the starbase database declared that miR-454-3p was interacted with HHEX. HHEX overexpression reversed the promotion of NSCLC cell proliferation and metastasis by exosomal miR-454-3p. CONCLUSIONS: Exosomal miR-454-3p enhanced the progression of NSCLC cells through HHEX. miR-454-3p may be a therapeutic target for NSCLC.
Serum vault RNA1-1 levels reflect blood cells and bone marrow.
Hatayama Y, Shimohiro H, Hashimoto Y … +3 more , Ichikawa H, Kawamura K, Motokura T
Mol Cell Probes · 2025 Apr · PMID 39924068 · Publisher ↗
INTRODUCTION: Vault RNA1-1 (vtRNA1-1) exhibits antiviral and anti-apoptotic effects in infected and malignant cells. We observed that vtRNA1-1 levels in serum fluctuate in patients with hematological disorders, but its e...
INTRODUCTION: Vault RNA1-1 (vtRNA1-1) exhibits antiviral and anti-apoptotic effects in infected and malignant cells. We observed that vtRNA1-1 levels in serum fluctuate in patients with hematological disorders, but its extracellular functions remain unclear. This study evaluates the potential of serum vtRNA1-1 levels as a biomarker for hematological disorders and investigates its association with bone marrow cell density (BMC). METHODS: Blood and serum samples were collected from patients with hematological disorders, patients who underwent bone marrow examination, PBSCT donors, and AML patients who received chemotherapy. VtRNA1-1 levels were measured using real-time quantitative RT-PCR. BMC was calculated by digital image analysis, and multiple regression analysis was performed using serum vtRNA1-1 and hematological and biochemical data as explanatory variables. RESULTS: The vtRNA1-1 levels in the blood of 11 patients with hematological disorders averaged 10.8 log cps/ml, significantly higher than 8.4 log cps/ml in serum. Multiple regression analysis estimated the vtRNA1-1 expression levels of each blood cell. In 87 patients who underwent bone marrow examination, there was a significant correlation between serum vtRNA1-1 levels and BMC (Rs = 0.24, P = 0.023). In PBSCT donors, serum vtRNA1-1 levels increased after G-CSF administration (P < 0.001), and in AML patients, serum vtRNA1-1 levels decreased after the initiation of chemotherapy, fluctuating in parallel with white blood cell counts. CONCLUSIONS: Our findings suggest that serum vtRNA1-1, derived from peripheral blood and bone marrow cells, can potentially serve as a clinical biomarker in specific diseases.
The role of APOA1-AS in colorectal cancer: Investigating its association with malignant biological behaviors.
Liu G, Zhao Q, Li Y … +2 more , Zhu D, Peng H
Mol Cell Probes · 2025 Apr · PMID 39889939 · Publisher ↗
PURPOSE: Colorectal cancer (CRC) is a common malignant tumor associated with high morbidity and mortality. Long non-coding RNAs (lncRNAs) play crucial roles in cancer development and progression. This study aimed to expl...
PURPOSE: Colorectal cancer (CRC) is a common malignant tumor associated with high morbidity and mortality. Long non-coding RNAs (lncRNAs) play crucial roles in cancer development and progression. This study aimed to explore the role of lncRNA APOA1-AS in colorectal cancer and elucidate its underlying mechanisms. METHODS: Clinical samples were collected, and high-throughput sequencing was performed to identify differentially expressed lncRNAs in colorectal cancer. Among these, the key lncRNA APOA1-AS was selected for further investigation. The expression of APOA1-AS in colorectal cancer tissues and cells was evaluated. The effects of APOA1-AS on cell proliferation, migration, invasion, and apoptosis were assessed through knockdown and overexpression of APOA1-AS in SW620 and RKO cells. Additionally, the relationship between APOA1-AS and the malignant biological behaviors of colorectal cancer cells was also investigated. Furthermore, the involvement of APOA1-AS in glucose metabolism reprogramming and the cGMP-PKG signaling pathway was analyzed. RESULTS: A total of 2985 differentially expressed lncRNAs were identified in colorectal cancer, including APOA1-AS, which showed the most significant upregulation. APOA1-AS expression was significantly higher in colorectal cancer tissues compared to normal tissues. Overexpression of APOA1-AS promoted cell proliferation, migration, and invasion while inhibiting apoptosis in SW620 and RKO cells. Furthermore, APOA1-AS was found to regulate glucose metabolism reprogramming, enhance tumor malignant biological behaviors and facilitate tumor cell drug resistance through the cGMP-PKG signaling pathway. CONCLUSION: Our study demonstrates that APOA1-AS is a potential key regulator in colorectal cancer development and progression. It functions via glucose metabolism reprogramming and the cGMP-PKG signaling pathway, offering a novel therapeutic target for colorectal cancer.
Circulating miR-574-5p shows diagnostic and prognostic significance and regulates oxygen-glucose deprivation (OGD)-induced inflammatory activation of microglia by targeting ATP2B2.
Yin X, Zhang C
Mol Cell Probes · 2025 Feb · PMID 39880338 · Publisher ↗
BACKGROUND: Early screening is critical for the prevention of ischemic stroke. miR-574-5p was considered a promising biomarker for ischemic stroke but lacks direct confirmation. This study evaluated miR-574-5p in discrim...
BACKGROUND: Early screening is critical for the prevention of ischemic stroke. miR-574-5p was considered a promising biomarker for ischemic stroke but lacks direct confirmation. This study evaluated miR-574-5p in discriminating ischemic stroke and predicting the severity and prognosis of patients, aiming to provide novel insights into the clinical prevention of ischemic stroke. METHODS: The clinical significance of miR-574-5p was evaluated in 103 ischemic stroke patients with 87 healthy individuals as control. The potential of serum miR-574-5p in the diagnosis and prognosis of ischemic stroke was assessed by ROC and logistic regression analyses. In vitro, oxygen-glucose deprivation (OGD)-induced microglia was established. The regulation of inflammation, oxidative stress, and proliferation of microglia by miR-574-5p were assessed by cell transfection. The downstream targets of miR-574-5p were predicted from public databases, and the targeting relationship was evaluated by luciferase reporter assay. RESULTS: Reducing serum miR-574-5p was observed in ischemic stroke patients relative to healthy individuals, which discriminated ischemic stroke patients. Serum miR-574-5p was negatively correlated with the NIHSS score of ischemic stroke patients and was identified as a risk factor for patients' adverse prognosis. In OGD-induced microglia, overexpressing miR-574-5p could alleviate OGD-induced inflammation and oxidative stress and promote cell growth. Among predicted targets, ATP2B2 was upregulated in ischemic stroke and showed a negative correlation with miR-574-5p. miR-574-5p negatively regulated ATP2B2 in OGD-induced microglia, and the overexpression of ATP2B2 reversed the protective effect of miR-574-5p. CONCLUSION: miR-574-5p acted as a biomarker for ischemic stroke and mediated neuroinflammation via targeting ATP2B2.
A comprehensive report of the clinical and mutational profiles of 30 Iranian malignant infantile osteopetrosis patients.
Amirfiroozy A, Naghinejad M, Rezamand A … +5 more , Farhangi H, Golchehre Z, Jalali H, Taheri M, Keramatipour M
Mol Cell Probes · 2025 Feb · PMID 39875016 · Publisher ↗
Osteopetrosis is a group of genetically and clinically diverse inherited disorders characterized by an increase in bone density. The main known cause is an abnormality in the development or function of osteoclasts. Hence...
Osteopetrosis is a group of genetically and clinically diverse inherited disorders characterized by an increase in bone density. The main known cause is an abnormality in the development or function of osteoclasts. Hence, the process of bone resorption is impaired, resulting in: 1- a reduction in bone marrow volume and, subsequently, a decrement in the hematopoietic capacity of bone marrow, which leads to anemia and compromised immunological function; 2- improper bone development, which leads to pressure on peripheral nerves, causing auditory, visual, and movement impairments; and 3- disturbance in the formation of bone microstructure that leads to susceptibility to bone fracture. This study aimed to evaluate the clinical symptoms and genetic causes of 30 patients (probands) who suffered from malignant infantile osteopetrosis, a subtype of this disorder. The Sanger sequencing technique was used to sequence four common genes (TCIRG1, CLCN7, SNX10, and OSTM1) in osteopetrosis. Subsequently, the selected variants were subjected to segregation analysis between the probands and their parents. Consequently, the sequencing of these four genes in probands revealed 16 pathogenic and likely pathogenic mutations, five of which had never been reported before. The TCIRG1 gene has three novel splice site variations and one frameshift variant. The CLCN7 gene had a novel missense variant. Also, a total of five variants of uncertain significance (VUSs) were identified in the analyzed sequences, of which three haven't been reported to date, and two were observed in osteopetrosis patients. Therefore, by documenting these novel likely pathogenic variants and VUS in known genes associated with this disease in patients, specialists can conduct more accurate genetic analysis and counseling when encountering these variants. Additionally, this documentation will facilitate the reclassification of these variants.
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