Molecular And Cellular Probes[JOURNAL]
Sun
200 papers
Reveal the regulatory role of DDX10 in diffuse large B-cell lymphoma: binding with FBL to promote cell proliferation and invasion.
Chen X, Chen W
Mol Cell Probes · 2026 Feb · PMID 41338403 · Publisher ↗
BACKGROUND: Diffuse large B cell lymphoma (DLBCL) is a heterogeneous malignancy with an unidentified molecular etiology. This study aims to investigate the role of DEAD-box helicase 10 (DDX10), a novel carcinogenic gene,...
BACKGROUND: Diffuse large B cell lymphoma (DLBCL) is a heterogeneous malignancy with an unidentified molecular etiology. This study aims to investigate the role of DEAD-box helicase 10 (DDX10), a novel carcinogenic gene, in DLBCL. METHODS: The expression of DDX10 in DLBCL was analyzed by the GEPIA2 bioinformatics tool. DDX10 and fibrillarin (FBL) expressions in DLBCL patients' cancer tissues and cell lines were measured via quantitative real-time reverse transcription polymerase chain reaction. RNA immunoprecipitation assay was used to confirm FBL-DDX10 interaction. The effects of DDX10/FBL overexpression and knockdown on cell viability, invasion, and Wnt/β-catenin pathway proteins were evaluated in DLBCL cell lines. RESULTS: DDX10 and FBL exhibited elevated expression levels in patients with DLBCL, particularly in those with stage III or IV DLBCL. DDX10 can bind to FBL in DLBCL cells. Silencing of DDX10 or FBL suppressed viability, proliferation and invasion, and downregulated the expressions of β-catenin, cyclin D1, and c-Myc proteins in DLBCL cells. The regulatory impact of DDX10 or FBL silencing on DLBCL cells was counteracted by the overexpression of FBL or DDX10. CONCLUSION: DDX10 contributes to the proliferation and invasion of DLBCL cells via positively regulating FBL, highlighting the DDX10-FBL axis as a potential therapeutic target. This work provides new insights into DLBCL pathogenesis and underscores the biomedical relevance of targeting DDX10-FBL.
Prognostic value of composite inflammatory prognostic model in pancreatic cancer.
Wei Q, Li Z, Feng H … +2 more , Zhang J, Wei L
Mol Cell Probes · 2025 Dec · PMID 41260275 · Publisher ↗
INTRODUCTION: Pancreatic cancer (PC) remains one of the most lethal malignancies worldwide, creating a critical need for reliable prognostic biomarkers, particularly those reflecting tumor microenvironment dynamics. METH...
INTRODUCTION: Pancreatic cancer (PC) remains one of the most lethal malignancies worldwide, creating a critical need for reliable prognostic biomarkers, particularly those reflecting tumor microenvironment dynamics. METHODS: We investigated the combined prognostic value of a composite inflammatory prognostic model for PC progression. A retrospective cohort analysis of 171 patients with PC was conducted using receiver operating characteristic (ROC) curve analysis, along with univariate and multivariate Cox regression analyses. Survival curves were plotted using the Kaplan-Meier method. A clinical prognostic nomogram was constructed based on independent prognostic factors. RESULTS: ROC curve analysis demonstrated that C-reactive protein-to-lymphocyte ratio (CLR) had the highest predictive accuracy for 3-year survival. Survival analysis revealed that TNM stage, CA19-9, CEA, neutrophil count, CRP level, the neutrophil-to-lymphocyte ratio (NLR), and CLR were significantly associated with overall survival. Multivariate Cox regression analysis confirmed that advanced lymphatic metastasis, advanced TNM stage, elevated CA19-9, elevated CEA, elevated neutrophil count, elevated NLR, and elevated CLR were independent prognostic factors. The prognostic nomogram incorporating these variables exhibited robust discriminative capacity and well-calibrated predictions of survival. Using the inflammatory prognostic model, patients in the high-risk group had a significantly shorter median overall survival than those in the low-risk group, with strong predictive accuracy for 1-year and 3-year survival. Validation in a subgroup of patients with pancreatic ductal adenocarcinoma further supported the clinical utility of the model, showing superior 3-year predictive performance and a pronounced survival disparity between the risk groups. CONCLUSIONS: A combination of inflammatory and clinical markers can effectively predict the prognosis of pancreatic cancer. The constructed composite inflammatory prognostic model demonstrated high clinical practical value and provided a reliable tool for individualized prognostic risk assessment.
Impact of preoperative clinical patient parameters on surgically obtained brain metastasis samples for translational research.
Rombach A, Geissler M, Xiao L … +17 more , Qasem LE, Stange L, Prinz V, Jussen D, Landolsi S, Kokkaliaris KD, Medyouf H, Sevenich L, Zeiner P, Reiss Y, Cakmak P, Armbrust M, Weber KJ, Plate KH, Offermanns S, Broggini T, Czabanka M
Mol Cell Probes · 2025 Dec · PMID 41197749 · Publisher ↗
Human tissue samples are a crucial resource for cancer research, offering key insights into physiological and pathological processes while enabling comprehensive characterization of molecular signatures across cancer sub...
Human tissue samples are a crucial resource for cancer research, offering key insights into physiological and pathological processes while enabling comprehensive characterization of molecular signatures across cancer subtypes. Recent advances in genetic analysis techniques lead to a substantiall expansion of specific molecular pathways knowledge. The application of these technologies to fresh tissue samples from patients undergoing surgical resection for metastatic disease represents a promising approach to gain a deeper understanding of the biology of brain metastasis. Brain metastases remain particularly challenging due to their poor prognosis and the complex mechanisms underlying central nervous system invasion. This study sought to identify preoperative factors influencing the research utility of fresh brain metastasis tissue samples. A pipeline was established to transfer fresh, surplus tissue from surgical resections to research laboratories with histological quality assessment. Of the fifty-five fresh specimens collected, thirty-eight (69 %) were classified as suitable for further research applications. Statistical analysis revealed that only two factors significantly affected sample quality. First, the extent of MRI-derived necrosis was significantly higher in unsuitable samples (mean 18.0 %) than in suitable samples (mean 8.3 %) (p = 0.0273). Second, prior treatment with target-specific therapeutics (TST) was associated with a lower proportion of suitable samples (47 %) compared to no prior TST (79 %) (p = 0.018). Logistic regression confirmed these variables as significant predictors, with MRI-derived necrosis (odds ratio 1.049) and target-specific therapy exposure (odds ratio 4.486) independently increasing the likelihood of obtaining suboptimal samples. Other parameters, including age, gender, metastasis volume, localization, primary cancer site, and other therapeutic interventions, showed no significant impact on sample quality. Based on these findings, the collection pipeline was modified to include evaluation by board-certified neuropathologists before samples are used for research purposes, improving the efficiency of translational research utilizing brain metastasis tissue.
Identification of lymphangiogenesis-related diagnostic model for predicting abdominal aortic aneurysm onset and progression and validation of lymphopoiesis in abdominal aortic aneurysm.
Qin S, Zhang J, Cao M … +2 more , Jiang T, Jiang B
Mol Cell Probes · 2026 Feb · PMID 41183720 · Publisher ↗
This study aims to explore the lymphangiogenesis (LG)-related diagnostic markers of abdominal aortic aneurysm (AAA) through bioinformatics, as well as the alteration of the regional lymphatic system during the progressio...
This study aims to explore the lymphangiogenesis (LG)-related diagnostic markers of abdominal aortic aneurysm (AAA) through bioinformatics, as well as the alteration of the regional lymphatic system during the progression of AAA and the influence of lymphatic drainage obstruction on AAA progression. 2957 differentially expressed genes (DEGs) were identified between the AAA patient group and the healthy donor group in Gene Expression Omnibus microarray datasets. Subsequently, the DEGs and the LG gene were intersected, and 93 genes were obtained. Weighted gene co-expression network analysis (WGCNA) was performed to obtain module genes. Module genes intersected with the above 93 genes, and 26 genes were obtained. Five hub genes (HSPA5, RAB10, RAB1A, RAF1, SMAD4) identified by machine learning may serve as diagnostic candidates for AAA patients through nomogram and ROC evaluation. Gene set enrichment analysis (GSEA) and immune infiltration analysis were performed further to understand the function of these candidate genes and explore the effect of immunity in AAA, respectively. By establishing an AAA animal model, it was found that the iliac lymph nodes around the abdominal aorta were significantly enlarged, and the number and lumen size of lymphatic vessels in the vessel wall were both significantly increased during the progression of AAA. Additionally, AAA was significantly promoted by ligating lymphatic vessels, which caused lymphatic drainage obstruction around the abdominal aorta. Our findings have the potential to enhance knowledge about the development and diagnosis of AAA.
Exploiting network-based drug repositioning to target metastasis in colorectal cancer: In-Silico prediction and in-vitro evidence.
Bazyari MJ, Firouzjaei AA, Ahmadi SM … +2 more , Khorashadizadeh M, Aghaee-Bakhtiari SH
Mol Cell Probes · 2025 Dec · PMID 41043568 · Publisher ↗
Metastasis is a major challenge in colorectal cancer (CRC) treatment. The incidence of regional and distant stages has increased during the past decade and the 5-year survival of metastatic CRC patients is 20 %. Although...
Metastasis is a major challenge in colorectal cancer (CRC) treatment. The incidence of regional and distant stages has increased during the past decade and the 5-year survival of metastatic CRC patients is 20 %. Although there is a necessity to develop systematic treatment, the cost and time of novel drug discovery hinder this progress. Drug repositioning simplifies this process by accelerating regulatory processes in drug discovery. Here we used a systems biology approach to find key player genes in the metastasis. First, we found differentially expressed genes in metastatic tissue compared to primary tumors. Then, we constructed and analyzed the protein-protein interaction (PPI) network to find hub genes and subjected them to query in the DrugBank database. We found plasminogen (PLG) is the hub gene in the constructed PPI network and tranexamic acid (TXA) is its known inhibitor with clinically approved antifibrinolytic activity. Pathway enrichment analysis showed that PLG is involved in matrix remodeling, Platelet activation, and cell energy production through insulin-growth factor uptake in colorectal cancer cells which are important processes during metastasis. We further explored the CPTAC-COAD proteomics data and found that the PLG level is significantly higher in stage IV compared to stage I. Interestingly, we found that PLG is correlated with mutation rate. We then investigated the effect of TXA on SW480 cells' mobility and migration by scratch assay and transwell migration assay. Both assays indicated that TXA can significantly inhibit the cells' migratory potential.
CRISPR/Cas as a tool to overcome drug resistance in cancer: From challenge to opportunity.
Hussen BM, Abdullah SR, Hidayat HJ … +5 more , Glassy MC, Safarzadeh A, Komaki A, Samsami M, Taheri M
Mol Cell Probes · 2025 Dec · PMID 41016566 · Publisher ↗
Drug resistance remains a significant challenge in cancer therapy, often resulting in treatment failure, tumor progression, and metastasis. The underlying resistance mechanisms-including genetic mutations, epigenetic alt...
Drug resistance remains a significant challenge in cancer therapy, often resulting in treatment failure, tumor progression, and metastasis. The underlying resistance mechanisms-including genetic mutations, epigenetic alterations, and modifications in drug efflux pathways-are complex and not yet fully understood. This review explores the application of CRISPR-Cas gene editing technology in understanding and overcoming drug resistance in cancer. It focuses on how CRISPR can identify and target resistance-associated genes to restore drug sensitivity. CRISPR-based approaches enable precise genetic modifications that offer new insights into the molecular basis of drug resistance. The technology has shown promise in dissecting resistance mechanisms and developing targeted therapeutic strategies. Nevertheless, key limitations such as inefficient delivery systems, off-target effects, and limited specificity hinder clinical translation. Current efforts focus on improving guide RNA design, creating more effective delivery vectors, and integrating CRISPR with existing treatments. CRISPR-Cas technology holds significant potential to address drug resistance in cancer by enabling targeted genetic interventions. Continued advancements are required to enhance its safety, specificity, and delivery, paving the way for its integration into future clinical applications.
Exosome biosensors for detection of ovarian cancer.
Vafadar A, Nayerain Jazi N, Eghtesadi M … +3 more , Ehtiati S, Movahedpour A, Savardashtaki A
Mol Cell Probes · 2025 Dec · PMID 40976549 · Publisher ↗
Ovarian cancer (OC) is one of the most aggressive gynecologic malignancies, largely due to its asymptomatic progression and frequent diagnosis at an advanced stage. Early detection is essential for improving patient surv...
Ovarian cancer (OC) is one of the most aggressive gynecologic malignancies, largely due to its asymptomatic progression and frequent diagnosis at an advanced stage. Early detection is essential for improving patient survival rates. Exosomes, small extracellular vesicles secreted by cells, are actively involved in OC progression and have been recognized as potential biomarkers for early diagnosis. Over the past decade, advancements in exosome research have emphasized the need for detection methods that are not only sensitive and reliable but also practical for clinical use. However, conventional approaches often face challenges such as limited sensitivity and complex sample preparation. Biosensors have emerged as a promising alternative, offering benefits such as non-invasiveness and improved analytical performance. This review examines recent developments in electrochemical, optical, and electrical biosensors for detecting OC-related exosomes, discussing their sensitivity, specificity, and potential applications in clinical settings.
Corrigendum to "Establishment of CRISPR/Cas9 lineage tracking technology for pig embryos" [Molecular and Cellular Probes 83 (2025) 102046].
Meng XQ, Xu XL, Gao Y … +1 more , Deng SL
Mol Cell Probes · 2026 Feb · PMID 40947334 · Publisher ↗
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Spatial and functional characterization of IL1RL1+ mast cells reveals immune regulatory roles in renal cancer.
Li Z, Zhang C, Ma K … +4 more , Han G, Song W, Yue M, Chen S
Mol Cell Probes · 2025 Dec · PMID 40912479 · Publisher ↗
BACKGROUND: Interleukin-1 receptor-like 1 (IL1RL1, also known as ST2) plays a critical role in immune regulation. Pan-cancer analysis has revealed that IL1RL1 is closely associated with cellular immune functions; however...
BACKGROUND: Interleukin-1 receptor-like 1 (IL1RL1, also known as ST2) plays a critical role in immune regulation. Pan-cancer analysis has revealed that IL1RL1 is closely associated with cellular immune functions; however, its role in clear cell renal cell carcinoma (ccRCC) and the tumor microenvironment (TME) remains poorly defined. METHODS: We analyzed IL1RL1 expression patterns using data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics (ST) were employed to investigate the cellular localization and biological functions of IL1RL1 in ccRCC. In addition, IL1RL1 knockout experiments were conducted to explore its potential role in antigen presentation. RESULTS: Compared to adjacent normal tissues, IL1RL1 expression was significantly downregulated in renal cancer tissues. Higher IL1RL1 expression correlated with improved patient prognosis, suggesting its potential as an independent prognostic biomarker. IL1RL1 was predominantly expressed in mast cells, with higher levels observed in adjacent normal tissues than in tumor tissues, implying a regulatory role in tumor immunity. Subset analysis revealed that IL1RL1-high mast cells were enriched in immune-inflammatory functions, including leukocyte activation, chemokine production, and antigen presentation. Cell-cell communication analysis further demonstrated that IL1RL1 mast cells may enhance CD8 cytotoxic T cell activation via the MHC-I signaling pathway. Spatial transcriptomics and multiplex immunohistochemistry (mIHC) confirmed the spatial co-localization of IL1RL1 mast cells and T cells within the TME. Furthermore, IL1RL1 knockout led to a reduction in HLA-A expression, providing functional evidence for its involvement in antigen presentation. CONCLUSION: Our findings highlight the immune-regulatory role of IL1RL1 mast cells in ccRCC. IL1RL1 may contribute to anti-tumor immunity through the modulation of antigen presentation and CD8 T cell activation, offering new insights into its potential as a prognostic biomarker and therapeutic target in renal cancer.
Non-coding RNAs in chronic lymphocytic leukemia: A systematic review and meta-analysis to decode the diagnostic potential.
Aghayan AH, Arab A, Haddadi S … +1 more , Atashi A
Mol Cell Probes · 2025 Dec · PMID 40886740 · Publisher ↗
BACKGROUND: Chronic lymphocytic leukemia (CLL) comprises around 25-30 % of leukemia cases in the West. Emerging evidence underscores the role of non-coding RNAs (ncRNAs) like miRNAs, lncRNAs, and CircRNAs in CLL pathogen...
BACKGROUND: Chronic lymphocytic leukemia (CLL) comprises around 25-30 % of leukemia cases in the West. Emerging evidence underscores the role of non-coding RNAs (ncRNAs) like miRNAs, lncRNAs, and CircRNAs in CLL pathogenesis and regulation. The unique properties of ncRNAs have given the potential as non-invasive diagnostic biomarkers for CLL. METHODS: PubMed, Web of Science, Scopus, ProQuest, and Embase databases were searched (from inception up to January 2024) for studies addressing the correlation of ncRNA expression levels with diagnosis of CLL. The QUADAS-2 tool was employed to evaluate the risk of bias in the included studies. The GRADE approach evaluated the certainty of the evidence for diagnostic test accuracy. RESULTS: A total of 14 studies including 934 CLL patients were analyzed. Evaluations focused on miRNAs and CircRNAs due to sufficient primary data. For miRNAs, pooled sensitivity: 0.84, specificity: 0.98, positive likelihood ratio (PLR): 42.19, negative likelihood ratio (NLR): 0.16, diagnostic odds ratio (DOR): 260.14; area under the curve (AUC): 0.96. For CircRNAs, pooled sensitivity: 0.69, specificity: 0.77, PLR: 3.01, NLR: 0.40, DOR: 7.51, AUC: 0.80. GRADE assessments indicated very low certainty of evidence for miRNAs and low certainty for CircRNAs. CONCLUSION: Both miRNAs and CircRNAs appear to hold promise as non-invasive diagnostic biomarkers in CLL, with miRNAs demonstrating higher diagnostic performance. However, based on the GRADE assessments, the certainty of evidence may undermine the reliability of the pooled estimates. Future studies with rigorous design, larger sample sizes, and standardized protocols are essential to strengthen the certainty of evidence.
Secreted clusterin inhibits keloid formation by promoting fibroblast apoptosis.
Niu Y, Zhang X, Chen Y … +3 more , Chen X, Liu X, Yao X
Mol Cell Probes · 2025 Oct · PMID 40854452 · Publisher ↗
Keloids are benign dermal proliferations resulting from excessive fibroblast activity that extends beyond the original site of injury. This study aims to investigate key biomarker genes associated with cell apoptosis and...
Keloids are benign dermal proliferations resulting from excessive fibroblast activity that extends beyond the original site of injury. This study aims to investigate key biomarker genes associated with cell apoptosis and proliferation in the pathogenesis of keloids. Bioinformatic analysis of Gene Expression Omnibus datasets identified 122 differentially expressed genes (DEGs) in samples from keloid patients. Following the intersection with apoptosis-related genes (ARGs), three DEGs-ANLN, CLU, and SFRP2-were identified as keloid-associated ARGs. Among these, the expression of CLU was consistently reduced across both training and validation datasets. Experimental validation confirmed the expression alteration of CLU in keloid patient samples and further revealed that the expression of secreted CLU (sCLU) was significantly decreased in keloid fibroblasts. At the same time, BAX was down-regulated while BCL2 was up-regulated. Overexpression of sCLU in keloid derived primary fibroblasts significantly promoted apoptosis and reduced the viability of the cells, accompanied with up-regulated BAX and down-regulated BCL2, and fibrotic factor genes, such as collagen I, collagen III, α-SMA and CTGF. In contrast, serum levels of CLU did not differ significantly between keloid patients and non-related controls, suggesting limited utility of circulating CLU as a diagnostic biomarker. Taken together, these findings reveal a crucial role of sCLU in keloid pathogenesis, thereby presenting a potential tissue-level biomarker for keloid diagnosis and a promising therapeutic target.
Establishment of CRISPR/Cas9 lineage tracking technology for pig embryos.
Meng XQ, Xu XL, Gao Y … +1 more , Deng SL
Mol Cell Probes · 2025 Oct · PMID 40816522 · Publisher ↗
Understanding tissue development in pigs is critical for biomedical research and genetic engineering, particularly for modeling human disease. However, tracing developmental origins and reconstructing lineage trees for p...
Understanding tissue development in pigs is critical for biomedical research and genetic engineering, particularly for modeling human disease. However, tracing developmental origins and reconstructing lineage trees for pig cells remains a significant challenge. Here, we present a high-resolution lineage tracing system that combines molecular barcoding with single-cell transcriptomics in pigs. Our system combines two key components: DNA barcodes (three CRISPR/Cas9 target sites and an 8-base pair intBC) integrated into the genome via piggyBac transposition, and a constitutive Cas9-EGFP cassette stably integrated at the Rosa26 locus using CRISPR/Cas12a. By combining lineage barcodes with single-cell RNA sequencing (scRNA-seq), we constructed an evolutionary lineage recorder that captures distinct cell states across developmental or differentiation trajectories. This system provides an essential tool for the subsequent construction of complete porcine cell fate maps. Our work provides a tool for studying porcine developmental biology, but also helps to optimize regenerative medicine strategies and improve the design of genetically engineered animal models.
Differential expression of lncRNAs in lung cancer subgroups.
Ataei S, Hussen BM, Kiani A … +3 more , Nazer N, Sayad A, Ghafouri-Fard S
Mol Cell Probes · 2025 Oct · PMID 40783102 · Publisher ↗
PURPOSE: Long non-coding RNAs (lncRNAs) have emerged as promising candidates in lung cancer research. This study aimed to assess the expression of eight autophagy-related lncRNAs in lung cancer tissues compared to matche...
PURPOSE: Long non-coding RNAs (lncRNAs) have emerged as promising candidates in lung cancer research. This study aimed to assess the expression of eight autophagy-related lncRNAs in lung cancer tissues compared to matched non-tumor samples and to evaluate their potential as diagnostic biomarkers. METHODS: We examined the expression levels of LINC01963, RAB11B-AS1, AC104083.1, PLBD1-AS1, AC005076.1, LOC105376805 (BX284668.5), AL132989.1, and HERPUD2-AS1 (AC018647.2) in lung cancer samples, including non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC), and compared them to their matched controls. Subgroup analyses were performed based on sex. RESULTS: All eight lncRNAs were upregulated in NSCLC samples compared with controls, with AC104083.1 and HERPUD2-AS1 showing the highest ratios of mean expression (19.86 and 14.60, respectively). In male patients, all lncRNAs were significantly overexpressed in tumor samples (p < 0.05), with AC104083.1 exhibiting the highest upregulation (ratio = 26.93). In female patients, although upregulation was observed, none of the lncRNAs reached statistical significance. In SCLC samples, most lncRNAs demonstrated strong upregulation trends; however, p-values ranged from 0.05 to 0.09, indicating borderline significance. PLBD1-AS1 showed the highest upregulation (ratio = 46.28), while LOC105376805 had minimal differential expression (ratio = 2.16, p = 0.23). Expression levels of these lncRNAs may help discriminate lung cancer samples from controls and could differentiate NSCLC from SCLC samples. CONCLUSION: These findings suggest that the evaluated lncRNAs have potential as diagnostic biomarkers, but further research is needed to confirm their utility.
Copy number variations in urine cell-free DNA from bladder neoplasm patients.
Haider CG, Wang Q, Wang G … +11 more , Wang Y, Fu Y, Zhang Z, Cao C, Xue F, Liu H, Wang Q, Zhou J, Jiang T, Cao J, Zhou Y
Mol Cell Probes · 2025 Oct · PMID 40684923 · Publisher ↗
Bladder cancer is a common malignancy, and its diagnosis is based on invasive procedures such as cystoscopy. Genetic aberrations play an important role in the development of many diseases, including bladder cancer. As a...
Bladder cancer is a common malignancy, and its diagnosis is based on invasive procedures such as cystoscopy. Genetic aberrations play an important role in the development of many diseases, including bladder cancer. As a result, identifying the genetic basis of a disease can provide useful information for early diagnosis and therapy. Cell-free DNA (cfDNA) offers a non-invasive approach to extract genetic information, which could be valuable for establishing the genetic cause of bladder cancer. In this study, we analyzed copy number variations (CNV) in urine cfDNA from 20 patients, with cystoscopy confirmed bladder cancer, sequenced by next-generation sequencing (NGS) and their CNV examined using the whole genome sequence. Statistical analysis of the carcinoma samples included Wilcoxon and Chi-square tests (p ≤ 0.005). Different patterns in CNV were identified in Chromosomes 1, 2, 3, 5, 6, 8, 9, 10, 11, 12, 17, 19, and 20 with the chromosome cytobands showing significant difference in variation patterns in patient parameters, such as smoking habit, number of tumors, grade of the tumors, and invasiveness. The genes that exhibited distinct CNV in each chromosomal cytoband have been associated with the development and progression of various cancers including bladder cancer indicating the clinical significance of CNVs as a useful tool for disease diagnosis. Therefore, this study demonstrates that by using NGS, CNV in urine cfDNA can provide valuable information on the state of blader cancer which can be further utilized to investigate therapies or early diagnosis.
Ubiquitin-specific peptidase 53 suppresses the tumorigenesis of breast cancer cells and its related gene analysis.
Lan H, Peng L, Chen F … +5 more , Xie K, Mu F, Wang J, Mei J, Yan W
Mol Cell Probes · 2025 Oct · PMID 40683612 · Publisher ↗
BACKGROUND: Breast cancer (BC) remains the most common malignancy affecting women's health globally. Thus, elucidating the molecular mechanisms driving BC progression and identifying novel therapeutic targets is imperati...
BACKGROUND: Breast cancer (BC) remains the most common malignancy affecting women's health globally. Thus, elucidating the molecular mechanisms driving BC progression and identifying novel therapeutic targets is imperative. Ubiquitin-specific peptidase 53 (USP53) is a deubiquitinating enzyme reported to exert tumor-suppressive effects in several types of cancers. However, USP53 has been poorly studied in BC. METHODS: Based on the TCGA database and GTEx transcriptome data, differentially expressed genes in BC were screened, and the relationship between USP53 expression and BC characteristics and prognosis were analyzed. qRT-PCR, Western blot, and immunohistochemistry determined USP53 expression. After transfection, BC cells' proliferation, migration, and invasion were assessed using CCK-8 and Transwell assay. A subcutaneous xenograft tumor model in nude mice was used to evaluate the in vivo effect of USP53. Besides, USP53 expression-associated immune cells were screened using the Cibersort package. RESULTS: USP53 expression was reduced in BC patients and showed potential diagnostic significance. Functionally, overexpressing USP53 inhibited BC cell proliferation, migration, and invasion, while silencing it promoted these malignant behaviors. In vivo, tumors derived from USP53-overexpressing cells grew more slowly and exhibited lower Ki67 expression. Additionally, we found that Tcm, T helper cells, Mast cells, and Eosinophils were positively associated with USP53 expression, whereas NK CD56dim cells and TReg were negatively associated with USP53 expression. CONCLUSIONS: Together, we proved that USP53 was down-regulated in BC and weakened the malignant progression of BC cells both in vitro and in vivo. USP53 was also associated with a variety of immune cells. Our study suggested that USP53 may be a novel target for BC therapy.
Single-cell sequencing revealed the recurrence causes of ETV6:RUNX1 fusion-positive B-ALL in children.
Guan G, Wang X, Li X … +12 more , Wang Q, Li X, Sun X, Liu L, Lu Y, Liu B, Li X, Zhao P, Gao F, Chen L, Zhao L, Dai Y
Mol Cell Probes · 2025 Oct · PMID 40659095 · Publisher ↗
OBJECTIVE: The ETV6RUNX1 fusion is the most common genetic abnormality in childhood B-cell acute lymphoblastic leukemia (B-ALL), yet nearly 50 % of relapses occur in patients initially classified as low-risk with this al...
OBJECTIVE: The ETV6RUNX1 fusion is the most common genetic abnormality in childhood B-cell acute lymphoblastic leukemia (B-ALL), yet nearly 50 % of relapses occur in patients initially classified as low-risk with this alteration. This study aimed to unravel the underlying pathways driving relapse in ETV6RUNX1 positive B-ALL. METHODS: Single-cell RNA sequencing (scRNA-seq) was performed on a cohort of four B-ALL patients with the ETV6RUNX1 fusion (three newly diagnosed and one relapsed case, selected from 25 patients). RESULTS: we discovered that relapsed samples exhibited a decline in T cell populations, an increase in CD8 Tex cells and B cells, and a higher proportion of malignant cells. Gene enrichment analysis demonstrated that IFN-γ response signaling pathways and inflammatory responses were significantly enriched in newly diagnosed samples. Conversely, the relapsed samples showed enrichment in the oxidative phosphorylation and glycolysis pathways. Additionally, analysis of cellular interactions revealed that malignant B cells could interact with T cells through LGALS9-HAVCR2, potentially leading to the exhaustion of effector T cells. Moreover, NPDC1, LEF1, and ERG exhibited higher activity levels in malignant B cells from relapsed patients, highlighting their roles in the progression and maintenance of leukemia. CONCLUSION: In summary, our study provides valuable insights into the potential causes of relapse in B-ALL patients with ETV6RUNX1, providing a foundation for the identification of prospective therapeutic targets.
RCN1 affects malignant progression and macrophage M2 polarization in diffuse large B-cell lymphoma.
Zhu Q, Yang X
Mol Cell Probes · 2025 Oct · PMID 40659094 · Publisher ↗
Malignant behaviors of cancer cells and immune evasion by macrophage can lead to treatment failure in diffuse large B-cell lymphoma (DLBCL). Recent studies have revealed the aberrant expression of reticulocalbin 1 (RCN1)...
Malignant behaviors of cancer cells and immune evasion by macrophage can lead to treatment failure in diffuse large B-cell lymphoma (DLBCL). Recent studies have revealed the aberrant expression of reticulocalbin 1 (RCN1) that is associated with malignant progression of several cancers. Nevertheless, its roles in DLBCL remain unclear. In this present study, several online bioinformatics databases substantiated high expression of RCN1 in tumor samples from DLBCL patients. Furthermore, there were obvious elevation of RCN1in tumor specimens form our collected tissues and DLBCL cells. Importantly, the shorter survival outcome was observed in patients with high levels of RCN1. Intriguingly, down-regulation of RCN1 attenuated DLBCL cell viability, invasion ability and increased cancer cell apoptosis. Moreover, TIMER database revealed the correlation between RCN1 expression and tumor-infiltrating macrophages, and M2 macrophage markers in DLBCL patients. Knockdown of RCN1 suppressed cancer cell ability to induce macrophage M2-like polarization by inhibiting the percentage of CD163 macrophages and expression of M2-like markers (CD163, CD204, and IL-10). Concomitantly, M2 macrophage-induced cancer cell viability and invasion was abrogated after RCN1 down-regulation. Further assay revealed that knockdown of RCN1 suppressed activation of the PI3K/AKT signaling in DLBCL cells. Notably, reactivation this pathway via its agonist 740Y-P offset the anti-tumor efficacy of RCN1 knockdown in cancer cell malignancy and macrophage polarization towards M2 phenotype. Therefore, RCN1 may contribute to the malignant progression of DLBCL by directly regulating cancer cell behavior and indirectly affecting macrophage M2-like polarization, supporting it as a promising therapeutic target against DLBCL.
Identification of CPLX1 expression as a potential prognostic marker in colorectal cancer.
Jin L, Qian L, Zhang X … +1 more , Liu T
Mol Cell Probes · 2025 Oct · PMID 40651544 · Publisher ↗
OBJECTIVES: CPLX1 is a member of the complexin/Synaphin family. Studies have shown that CPLX1 is involved in tumor progression. However, the biological mechanism by which CPLX1 is involved in colorectal cancer (CRC) is u...
OBJECTIVES: CPLX1 is a member of the complexin/Synaphin family. Studies have shown that CPLX1 is involved in tumor progression. However, the biological mechanism by which CPLX1 is involved in colorectal cancer (CRC) is unclear. METHODS: TIMER and TCGA database provided difference expression of CPLX1 mRNA in pan-cancer and CRC. We collected 90 cases of CRC and adjacent normal tissues for immunohistochemistry (IHC) and investigated CPLX1 protein expression and its correlation with clinical information. Cox regression and Kaplan-Meier were conducted to determine prognostic value of CPLX1 expression. We utilized Spearman analysis to explore the association between CPLX1 and immune cell infiltration, immune checkpoints. We utilized GSEA to investigate the biological molecular function for CPLX1 in CRC. RESULTS: CPLX1 mRNA expression was elevated in several cancers, including CRC. Elevated CPLX1 protein expression was confirmed by IHC in CRC samples, and showed a positive association with T stage. The survival analysis demonstrated that CPLX1 overexpression was linked to a poorer overall survival (OS), disease-specific survival (DSS), and progress-free interval (PFI) for CRC. Time ROC analysis suggested that the survival rate of 1-year, 2-year and 3-year for OS, DSS, and PFI was above 0.5, suggesting a certain prognostic value in CRC. Cox regression considered CPLX1 expression as a good prognostic index for predicting OS, DSS, and PFI. Furthermore, CPLX1 expression was associated with immunity in CRC. Functional analysis showed that CPLX1 related genes had participation in Notch signaling pathway. CONCLUSIONS: CPLX1 was a latent prognostic and diagnostic marker for CRC and may also be a potential therapeutic target.
Progress in the pathogenesis and treatment of pituitary neuroendocrine tumors (PitNETs): From molecular mechanisms to emerging therapies.
Wu N, Wu N, Wang N … +1 more , Zhu Y
Mol Cell Probes · 2025 Oct · PMID 40581303 · Publisher ↗
Pituitary neuroendocrine tumors (PitNETs), arising from anterior pituitary neuroendocrine cells, constitute 10-15 % of intracranial tumors. Though mostly benign, their location near critical structures like the optic chi...
Pituitary neuroendocrine tumors (PitNETs), arising from anterior pituitary neuroendocrine cells, constitute 10-15 % of intracranial tumors. Though mostly benign, their location near critical structures like the optic chiasm and cavernous sinus causes severe neuroendocrine dysfunctions and mass effects. The 2022 WHO classification rebranded them from "pituitary adenomas" to emphasize their neuroendocrine lineage, yet challenges in prognostic prediction retain traditional terminology. Pathogenesis involves genetic mutations GNAS in GH-PitNETs, USP8 in ACTH-PitNETs), epigenetic dysregulation (METTL3-mediated m6A methylation), and signaling pathway aberrations (cAMP-PKA activation). Current treatments-surgery, dopamine agonists, somatostatin analogs, and radiation-face limitations like recurrence and side effects. Emerging strategies include targeted therapies (BET inhibitors) and immune checkpoint blockade, but tumor heterogeneity and lack of predictive biomarkers remain key obstacles. This review synthesizes pathogenesis, therapeutic advances, and research gaps to foster precision medicine and novel diagnostic/treatment paradigms for PitNETs.
Assessment of cancer-associated fibroblast signature genes in ovarian cancer patients: impact on immunity, drug resistance, and prognosis.
Zhang S, Yan J, Pan W … +6 more , Jia C, Liu W, Liu S, Wang Z, Liu Y, Zhang Y
Mol Cell Probes · 2025 Oct · PMID 40541693 · Publisher ↗
Ovarian cancer (OC) is women's third most common gynecologic tumor and is highly lethal. Cancer-associated fibroblasts (CAFs) are associated with cancer at all stages of disease progression and are involved in biological...
Ovarian cancer (OC) is women's third most common gynecologic tumor and is highly lethal. Cancer-associated fibroblasts (CAFs) are associated with cancer at all stages of disease progression and are involved in biological processes, including inflammatory processes, tumor development occurrence, and immune rejection. This study aimed to construct prognosis-related CAFs regulatory factors to predict the survival of OC patients. Datasets of OC patients with complete clinical information were collected from the Gene Expression Omnibus (GEO) and the Cancer Genome Atlas (TCGA) databases. First, we identified potential regulator factors of CAFs in OC based on the xCell algorithm and weighted gene co-expression analysis (WGCNA). Further screening using one-way cox regression analysis and LASSO regression models yielded 22 prognosis-related CAFs regulatory factors, using which a model was constructed. Subsequently, the diagnostic effectiveness of the model was assessed using receiver operating characteristic (ROC) curves, and the validity of the CAFs regulatory factors survival model was verified in three additional independent datasets and single cell data. Meanwhile, experimental validation was conducted using immunohistochemistry and Western blot. The results showed that GAS1 (Growth arrest specific 1) exhibited a higher expression pattern in fibroblasts from ovarian cancer patients. The assessment of resistance and immune checkpoint differences across various risk score groups indicates that the CAFs regulatory factor survival model is practical for guiding systemic treatment. In summary, this study establishes a prognostic model composed of 22 CAFs regulatory factors to predict the prognosis of ovarian cancer (OC), providing new perspectives for the clinical treatment of OC.
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