OBJECTIVE: The aim was to investigate the clinical performance of microRNA-199a-3p (miR-199a-3p) in patients with chronic periodontitis. METHODS: 91 patients with chronic periodontitis and 78 healthy individuals were enr...OBJECTIVE: The aim was to investigate the clinical performance of microRNA-199a-3p (miR-199a-3p) in patients with chronic periodontitis. METHODS: 91 patients with chronic periodontitis and 78 healthy individuals were enrolled for the research subjects. MiR-199a-3p expression was detected using real-time quantitative PCR (RT-qPCR) assay. Pearson correlation analysis was used for the relevance of miR-199a-3p with inflammatory mediators. Receiver operating characteristic (ROC) and logistic regression were conducted for the evaluation of the diagnostic performance and risk factors of chronic periodontitis. Bioinformatics analysis was utilized for miR-199a-3p-related genes. RESULTS: MiR-199a-3p was distinctly decreased in gingival crevicular fluid from patients with chronic periodontitis. The area under the curve (AUC) was 0.978 to discriminate chronic periodontitis patients from healthy individuals. The negative correlation was observed between miR-199a-3p and inflammatory factors. Logistic regression showed that miR-199a-3p was an independently protective factor for the occurrence of chronic periodontitis. Bioinformatics analysis revealed that the predictive regulated genes of miR-199a-3p mainly concentrated in inflammatory-associated signaling pathways. CONCLUSION: MiR-199a-3p was attenuated in patients with chronic periodontitis and an underlying diagnostic biomarker for the disease.
Despite numerous attempts to understand the molecular mechanisms behind the development of liver cancer, it continues to pose a significant worldwide health challenge. Transcriptome sequencing, a powerful tool in molecul...Despite numerous attempts to understand the molecular mechanisms behind the development of liver cancer, it continues to pose a significant worldwide health challenge. Transcriptome sequencing, a powerful tool in molecular biology, has played a pivotal role in uncovering the intricate gene expression profiles underlying hepatocellular carcinoma (HCC). In the present study, we identified a total of 808 differentially expressed genes (DEGs), with 584 exhibiting downregulation, and 224 showing upregulation following apigetrin treatment. We utilized a combination of bioinformatics tools and platforms, including Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment and mapping, Protein-Protein Interaction (PPI), and GEPIA. We found that DEGs were related to the apoptotic cell death process and identified hub genes, namely CASP8, RB1, and TGFBR2. These genes were further validated through both GEPIA analysis and western blot experiments. Our findings collectively demonstrate that apigetrin has the potential to modulate genes related to liver cancer and trigger molecular pathways that lead to apoptotic cell death in liver cancer cells. This study underscores the potential of apigetrin as an innovative treatment strategy for HCC, emphasizing the need for additional research to elucidate its mechanisms of action and evaluate its clinical efficacy.
Ferroptosis is a regulated cell death mechanism distinct from apoptosis, autophagy, and necroptosis, marked by iron accumulation and lipid peroxidation. Since its identification in 2012, it has developed into a potential...Ferroptosis is a regulated cell death mechanism distinct from apoptosis, autophagy, and necroptosis, marked by iron accumulation and lipid peroxidation. Since its identification in 2012, it has developed into a potential therapeutic target, especially concerning GI disorders like PC, HCC, GC, and CRC. This interest arises from the distinctive role of ferroptosis in the progression of diseases, presenting a new avenue for treatment where existing therapies fall short. Recent studies emphasize the promise of focusing on ferroptosis to fight GI cancers, showcasing its unique pathophysiological mechanisms compared to other types of cell death. By comprehending how ferroptosis aids in the onset and advancement of GI diseases, scientists aim to discover novel drug targets and treatment approaches. Investigating ferroptosis in gastrointestinal disorders reveals exciting possibilities for novel therapies, potentially revolutionizing cancer treatment and providing renewed hope for individuals affected by these tumors.
BACKGROUND: ARPC1B has been identified as a key regulator of malignant biological behavior in various tumors. However, its specific role in clear cell renal cell carcinoma (ccRCC) remains poorly understood. This study ai...BACKGROUND: ARPC1B has been identified as a key regulator of malignant biological behavior in various tumors. However, its specific role in clear cell renal cell carcinoma (ccRCC) remains poorly understood. This study aims to evaluate the influence of ARPC1B on the prognosis and disease progression in ccRCC patients. METHODS: Multi-omics data and clinical information from public databases were analyzed to determine the associations between ARPC1B and prognosis, clinical features, immune microenvironment, and drug sensitivity in ccRCC. Co-expression and gene set enrichment analyses were conducted to elucidate the potential role of ARPC1B in ccRCC pathogenesis. Functional assays, including RT-qPCR, CCK8 assays, colony formation assays, immunofluorescence, immunohistochemistry, and xenograft tumor formation in nude mice, were performed to assess ARPC1B's impact on cell proliferation and apoptosis. Flow cytometry and Western blotting were further employed to investigate the underlying molecular mechanisms of ARPC1B in ccRCC. RESULTS: ARPC1B expression was significantly elevated in ccRCC and associated with an unfavorable prognosis. Both independent and meta-analyses confirmed that ARPC1B is an independent prognostic risk factor in ccRCC. Furthermore, ARPC1B expression significantly correlated with the immune microenvironment and drug sensitivity. In vitro, experiments demonstrated that ARPC1B knockdown suppressed ccRCC cell proliferation and induced apoptosis through the BAX-Bcl-2/c-caspase3/c-PARP axis, which was further validated by in vivo studies. CONCLUSION: ARPC1B overexpression is associated with poor prognosis, altered immune status, and drug sensitivity in ccRCC. Furthermore, ARPC1B promotes the malignant behavior of ccRCC cells and holds potential as a prognostic biomarker and therapeutic target for ccRCC.
The rapid advancements in the field of genetics have significantly propelled the development of gene therapies, paving the way for innovative treatments of various hereditary disorders. This review focuses on the genetic...The rapid advancements in the field of genetics have significantly propelled the development of gene therapies, paving the way for innovative treatments of various hereditary disorders. This review focuses on the genetics of ophthalmologic conditions, highlighting the currently approved ophthalmic gene therapy and exploring emerging therapeutic strategies under development. Inherited retinal dystrophies represent a heterogeneous group of genetic disorders that manifest across a broad spectrum from infancy to late middle age. Key clinical features include nyctalopia (night blindness), constriction of the visual field, impairments in color perception, reduced central visual acuity, and rapid eye movements. Recent technological advancements, such as multimodal imaging, psychophysical assessments, and electrophysiological testing, have greatly enhanced our ability to understand disease progression and establish genotype-phenotype correlations. Additionally, the integration of molecular diagnostics into clinical practice is revolutionizing patient stratification and the design of targeted interventions, underscoring the transformative potential of personalized medicine in ophthalmology. The review also covers the challenges and opportunities in developing gene therapies for other ophthalmic conditions, such as age-related macular degeneration and optic neuropathies. We discuss the viral and non-viral vector systems used in ocular gene therapy, highlighting their advantages and limitations. Additionally, we explore the potential of emerging technologies like CRISPR/Cas9 in treating genetic eye diseases. We briefly address the regulatory landscape, concerns, challenges, and future directions of gene therapy in ophthalmology. We emphasize the need for long-term safety and efficacy data as these innovative treatments move from bench to bedside.
Gastric cancer (GC), among the most prevalent malignant tumors globally, demonstrates a rapid metastasis rate leading to high mortality. While microRNAs (miRNAs) have been recognized as critical regulators of tumor progr...Gastric cancer (GC), among the most prevalent malignant tumors globally, demonstrates a rapid metastasis rate leading to high mortality. While microRNAs (miRNAs) have been recognized as critical regulators of tumor progression, the specific role of miR-28-3p in GC remains unclear. In this study, we demonstrate that miR-28-3p acts as a tumor suppressor by inhibiting GC cell proliferation and EMT-driven migration in vitro, as well as tumor growth and metastasis in vivo. Mechanistically, miR-28-3p directly targets ADP ribosylation factor 6 (ARF6), a small GTPase identified as an oncogene in GC. We reveal that ARF6 is significantly upregulated in GC and activates the GLI1/2-dependent Hedgehog signaling pathway, promoting tumor growth and EMT. Notably, ARF6 knockdown mitigates the pro-tumor effects caused by miR-28-3p deficiency, while combined ARF6 inhibition and Hedgehog pathway suppression exhibit synergistic anti-tumor effects. This study establishes the miR-28-3p-ARF6-Hedgehog signaling axis as a critical regulatory pathway in GC progression. Our findings provide novel insights into GC pathogenesis and highlight the therapeutic potential of targeting this axis for innovative treatment strategies.
Long non-coding RNA TMC3-AS1 is identified to be upregulated by lipopolysaccharide (LPS) in inflammatory disease, but its role in acute kidney injury (AKI) is almost unknown. The study investigated the involvement of TMC...Long non-coding RNA TMC3-AS1 is identified to be upregulated by lipopolysaccharide (LPS) in inflammatory disease, but its role in acute kidney injury (AKI) is almost unknown. The study investigated the involvement of TMC3-AS1 in LPS-induced AKI and its downstream molecular regulatory mechanism. Our data suggested that knocking down TMC3-AS1 significantly reduced renal dysfunction, tissue inflammation and tissue damage in LPS-induced mice, and promoted cell viability, inhibited inflammation, apoptosis and necrosis in LPS-stimulated human renal tubular epithelial cells HK2. Meanwhile, silencing TMC3-AS1 decreased the expression levels of Wnt5a, Atg5, NLRP3 and cleaved caspase1 and the ratio of LC3II/LC3I, but elevated p62 level in vivo and in vitro, suggesting the inhibitory effect of TMC3-AS1 silence on Wnt5a signaling, autophagy, and pyroptosis. Mechanically, TMC3-AS1 upregulated the expression of WNT5A mRNA and Wnt5a protein through competitively binding with miR-148a-3p, thus elevating the expression levels of autophagy and pyroptosis-associated markers in LPS-induced HK2 cells. MiR-148a-3p mimic also exerted protective effects on LPS-treated HK2 cells, which was counteracted by overexpressing WNT5A or TMC3-AS1. Altogether, these findings reveal that TMC3-AS1 inhibition restrains LPS-triggered AKI progression through inactivating Wnt5a -mediated autophagy and pyroptosis pathway.
BACKGROUND: breast cancer-associated fibroblast (CAF) is linked to metastasis and is poor for breast cancer prognosis. Since Clostridium Toxin A (Botox-A) had represented a cytotoxic effect on fibroblasts, this study aim...BACKGROUND: breast cancer-associated fibroblast (CAF) is linked to metastasis and is poor for breast cancer prognosis. Since Clostridium Toxin A (Botox-A) had represented a cytotoxic effect on fibroblasts, this study aims to assess Botox-A cytotoxicity in both normal fibroblasts and exosome-induced CAFs. MATERIAL AND METHOD: the serum exosomes of 40 BC patients and 30 healthy individuals were isolated and lncRNA H19 (lnch19) levels were assessed by qRT-PCR method. After that, Breast Cancer (BC) exosomes co-cultured with Human foreskin fibroblasts (HFF) and qRT-PCR were applied to evaluate α-SMA, Vimentin, BCL-2, and BAX expression. Both Normal and malignant HFFs co-cultured with Botox-A, and Botox-A loaded exosome for 24 and 48 h and their apoptosis, Cell proliferation, and viability were monitored by MTT assay, Annexin V-FITC and PI staining and qRT-PCR for BCL-2, BAX, and cyclin D1 mRNAs. RESULTS: Serum exosomes of BC patients had significantly higher levels of lncRNA H19 than healthy individuals. MTT assay results showed Botox-A decreased vital Human foreskin fibroblasts in a dose-dependent manner. BC exosomes significantly increased α-SMA, Vimentin, and BCL-2 mRNA levels in Human foreskin fibroblasts, on the other hand, BAX decreased meaningfully. Co-culture of exosome-treated HFF cells with both Botox-A and Botox-A loaded exosomes significantly boosted BCL-2 mRNA levels, completely contrary to BAX and cyclid d1 expression. Meanwhile, flow cytometry results confirmed a high rate of apoptosis in malignant Human foreskin fibroblasts treated with Botox-A loaded exosome. CONCLUSION: The findings of this study indicate that exosomal lncRNA H19 could be a diagnostic marker for Breast Cancer and these Breast cancer exosomes can induce malignant phenotype in fibroblasts and turn them into CAFs. Botox-A could be toxic for both normal fibroblasts and CAFs, inducing apoptosis and suppressing cell proliferation among them.
Myotonic dystrophy type 1 (DM1) is a serious multisystem disorder caused by GCA repeat expansions in the DMPK gene. Early and accurate diagnosis, often requiring reliable DNA-diagnostic techniques, is critical for preven...Myotonic dystrophy type 1 (DM1) is a serious multisystem disorder caused by GCA repeat expansions in the DMPK gene. Early and accurate diagnosis, often requiring reliable DNA-diagnostic techniques, is critical for preventing life-threatening cardiac complications. Clinically, two main diagnostic challenges exist. Firstly, because of overlapping symptomatology with other conditions, conventional DNA-testing methods focusing on DM1 expansion detection ensure diagnostic results only in a small subset of patients, and frequently, further DNA-testing in remaining cases is necessary. Secondly, because of variable symptomatology and age of onset, not all DM1 patients are referred for DM1 genetic testing, leading to unrecognized but at-risk cases. When using conventional methods, the main technical problems are expanded-allele sizing and sensitivity to the presence of sequence interruptions. On a set of 50 individual genomes, including ten DM1 patients, we tested the performance of short-read whole-genome sequencing (WGS), one of the most up-to-date molecular testing methods. We identified all expansion-range DM1 alleles and characterized sequence interruptions in seven expansion-range/premutation-range alleles. Although neither the tested conventional methods, nor WGS allowed expanded-allele sizing, conventional methods provided higher sizing limits for normal-range alleles. Genotyping concordance rate was found to be 95-99 %. WGS was found to be superior in elucidating the sequence structure of the motifs, even if they fall outside the sizing limit (from partial reads). In addition, WGS enables the identification of genetic modifiers in other genes and the detection of alternative diagnoses in DM1-negative patients by extension of the bioinformatic evaluation of the generated data.
BACKGROUND: Thrombospondin 1 (THBS1), a secreted protein, is implicated in the progression of numerous cancers, yet its specific contributions to pancreatic cancer (PC) remain underexplored. METHODS: The association betw...BACKGROUND: Thrombospondin 1 (THBS1), a secreted protein, is implicated in the progression of numerous cancers, yet its specific contributions to pancreatic cancer (PC) remain underexplored. METHODS: The association between THBS1 levels and prognosis in PC was investigated. Functional experiments in vitro were used to determine the cell functions of siTHBS1 through CCK8 assay for cell proliferation, Muse® Cell Analyzer for apoptosis, and transwell assay for invasion and migration. Colivelin was applied in recovery experiment to investigate the mechanism of THBS1 regulating the JAK2/STAT3 pathway in BXPC-3 cell. In addition, the LV-shTHBS1 lentivirus was used to construct subcutaneous tumors in nude mice to verify the function of THBS1 in vivo. RESULTS: THBS1 expression was elevated in PC and associated with a poorer prognosis. THBS1 was highly expressed in these PC cells. siTHBS1 repressed cell growth, migration and invasiveness, while promoting apoptosis of BXPC-3 cells. THBS1 suppression also led to a decrease in the phosphorylation of JAK2 and STAT3. JAK2/STAT3 signaling activator (Colivelin) could partially reverse the biological effects. In addition, shTHBS1 can suppress the growth of implanted tumors in nude mice. CONCLUSIONS: THBS1 knockdown suppressed cell proliferation, migration, and invasion while enhanced cell apoptosis through the JAK2/STAT3 signaling pathway.
High-throughput genetic screening serves as an indispensable approach for deciphering gene functions and the intricate relationships between phenotypes and genotypes. The CRISPR/Cas9 system, with its ability to precisely...High-throughput genetic screening serves as an indispensable approach for deciphering gene functions and the intricate relationships between phenotypes and genotypes. The CRISPR/Cas9 system, with its ability to precisely edit genomes on a large scale, has revolutionized the field by enabling the construction of comprehensive genomic libraries. This technology has become a cornerstone for genome-wide screenings in disease research. This review offers a comprehensive examination of how CRISPR/Cas9-based genetic screening has been leveraged to uncover genes that play a role in disease mechanisms, focusing on areas such as cancer development and viral replication processes. The insights presented in this review hold promise for the development of novel therapeutic strategies and precision medicine approaches.
Descurainia sophia, as an an ethno-medicinal plant, contains antioxidant compounds that safeguard cellular integrity against various forms of damage and may play a role in cancer prevention. Antioxidant compounds present...Descurainia sophia, as an an ethno-medicinal plant, contains antioxidant compounds that safeguard cellular integrity against various forms of damage and may play a role in cancer prevention. Antioxidant compounds present in this plant facilitate the body's production of new cells and diminish the risk of colon cancer. In recent years, silver nanoparticles synthesized through green methods using ethnomedicinal herbs have been employed in cancers treatment. We have conducted an investigation into silver nanoparticles that were synthesized through green chemistry principles, utilizing the Descurainia sophia leaves extract for lung carcinoma treatment. The efficacy of Ag NPs against prevalent lung cancer cells was assessed. The green-synthesized silver nanoparticles characterization was conducted utilizing X-ray diffraction (XRD), field emission scanning electron microscopy (FE-SEM), ultraviolet-visible spectroscopy (UV-Vis), energy-dispersive X-ray spectroscopy (EDX), and transmission electron microscopy (TEM). The findings from morphological analyses validate the nanoparticles spherical shape, which ranges in size from 20 to 60 nm. The IC values were determined to be 173, 125, and 109 μg/mL for HLC-1, LC-2/ad, and PC-14 cell lines, respectively. According to recent data, Ag NPs may be a useful option to support the treatment of lung cancer. Although the current study presents encouraging findings, further investigation is necessary to gain a deeper understanding of the mechanisms of action and potential side effects of silver nanoparticles on HUVEC cells.
bla is the only widely found β-lactamase in Neisseria meningitidis, and its presence is on the rise. To enhance our bacterial meningitis testing procedure, we clinically validated a real-time PCR assay to rapidly detect...bla is the only widely found β-lactamase in Neisseria meningitidis, and its presence is on the rise. To enhance our bacterial meningitis testing procedure, we clinically validated a real-time PCR assay to rapidly detect the bla gene and predict drug resistance in Neisseria meningitidis. A screen of 101 clinical isolates and 37 clinical specimens of blood and cerebrospinal fluid received between January 2018 and June 2024 found 8 isolates and 2 cerebrospinal fluid specimens that were positive for bla.
BACKGROUND: Due to the complex pathogenesis of endometriosis, its early screening and development prediction are still challenging problems in the clinic. OBJECTIVES: This study evaluated the significance of miR-375-3p i...BACKGROUND: Due to the complex pathogenesis of endometriosis, its early screening and development prediction are still challenging problems in the clinic. OBJECTIVES: This study evaluated the significance of miR-375-3p in endometriosis onset, progression, and recurrence, aiming to identify a novel biomarker for disease diagnosis and prognosis. MATERIALS AND METHODS: The study enrolled 100 patients with endometriosis and 80 healthy females. The serum miR-375-3p levels were compared between the two groups, and its diagnostic significance and predictive value were assessed by ROC and Cox regression analyses. The effect of miR-375-3p on endometriosis cell growth and motility was evaluated by CCK8 and Transwell assays. RESULTS: Endometriosis patients showed a lower serum miR-375-3p level relative to healthy females, and more severe the disease condition, lower the miR-375-3p in endometrial tissues is. Reducing serum miR-375-3p could discriminate endometriosis patients sensitively and specifically. Additionally, miR-375-3p was identified as a predictor for the recurrence of endometriosis together with stage, lesion size, and the levels of related hormones. In endometriosis cells, miR-375-3p was demonstrated to target NOX4 and negatively regulated its expression. Overexpressing miR-375-3p significantly suppressed cell proliferation, migration, and invasion, which was reversed by NOX4. CONCLUSION: Decreasing miR-375-3p served as a biomarker for endometriosis onset, development, and recurrence. miR-375-3p regulated endometriosis cell growth and motility via negatively modulating NOX4.
Ciprofloxacin (CIP) is a broad-spectrum fluoroquinolone antibiotic, and its excessive residues in food and water sources pose potential risks to human health. Therefore, there is a need for a rapid and convenient method...Ciprofloxacin (CIP) is a broad-spectrum fluoroquinolone antibiotic, and its excessive residues in food and water sources pose potential risks to human health. Therefore, there is a need for a rapid and convenient method for its accurate quantification. The clustered regularly interspaced short palindromic repeat (CRISPR)/Cas12a system has gained extensive application in signal detection and amplification due to the trans-cleavage activity of Cas12a. In this study, we devised a novel magnetic bead-based dual sandwich aptamer coupled with a CRISPR/Cas12a system for the precise quantification of CIP in milk, river water, and honey. Through the incorporation of a magnetic bead-based dual aptamer sandwich approach, the concentration of CIP in the samples was pre-enriched. Additionally, by optimizing the Fluorescence-Quencher (F-Q) probe concentration, detection aptamer (APTd) concentration, and assay duration, the limit of blank (LOB) of the system was determined as 362 nM, while the limit of detection (LOD) was determined as 403 nM. This enabled the accurate quantification of CIP within the linear range of 0.5 μM to 0.2 mM with high specificity. Moreover, the performance of this detection method was comparable to that of high-performance liquid chromatography (HPLC) in river water, milk, and honey samples.
The therapeutic potential of intestinal stem cell-derived extracellular vesicles (ISCs-EVs) in necrotizing enterocolitis (NEC) remains largely unexplored. This research aims to investigate the therapeutic effects of ISCs...The therapeutic potential of intestinal stem cell-derived extracellular vesicles (ISCs-EVs) in necrotizing enterocolitis (NEC) remains largely unexplored. This research aims to investigate the therapeutic effects of ISCs-EVs on NEC. Lgr5-positive ISCs were screened from the small intestine of mice by flow cytometry, and ISCs-EVs were isolated by density gradient centrifugation. Subsequently, ISCs-EVs were identified through transmission electron microscopy, nanoparticle tracking analysis, and western blotting. Subsequently, we evaluated the efficacy of ISCs-EVs in a mouse model of NEC and found that they enhanced survival (more than 20 %), reduced intestinal damage (restore the number of intestinal crypts and decrease the expression of MPO and cleaved-caspase 3 in intestinal tissues), promoted angiogenesis (the mRNA expression of VEGF was increased by approximately 35 %), and mitigated inflammation (decreased the level of MUC1, p-NF-κB, IL-6 and TNF-α). Furthermore, in vitro assessments demonstrated that ISCs-EVs reduced apoptosis (P < 0.01) and stimulated proliferation (P < 0.05) of IEC-6 cells, while enhancing mucin secretion in LS174T cells. In summary, our study provides a comprehensive assessment of the therapeutic effects of ISCs-EVs on NEC, using both animal and cell models. This highlights their potential for use in NEC treatment.
AIM: The metabotropic glutamate receptor, GRM7 is a gene in the neurotransmitters prognostic signatures. Downregulation of this gene is associated with the progression of glioma tumors and has a negative impact on the im...AIM: The metabotropic glutamate receptor, GRM7 is a gene in the neurotransmitters prognostic signatures. Downregulation of this gene is associated with the progression of glioma tumors and has a negative impact on the immune response. METHODS: In the present study, we aim to assess the associations between rs6782011 and rs779867 SNPs within this gene and risk of glioblastoma multiforme (GBM) in Iranian population. RESULTS: There was a noteworthy difference in distribution of genotypes (P value = 0.001) and alleles (P value = 0.0002) of rs779867 between total GBM cases (n = 299) and total normal controls (n = 302). In addition, the significant difference in genotypes and alleles distribution was observed for both male and female GBM cases vs. respective normal controls. For rs6782011 variant, the significant difference in genotypes distribution was observed between male GBM cases (n = 187) vs. respective normal controls (n = 156) (P value = 0.004) and between total GBM cases (n = 299) vs. total normal controls (n = 302) (P value = 0.02). However, there was no significant difference in genotypes distribution between female GBM cases and respective normal controls (P value = 0.1). Distribution of rs6782011 alleles was not different between total GBM cases and normal controls; and between male GBM cases and male normal controls. However, there was a significant difference in alleles distribution between female GBM cases and female normal controls. CONCLUSION: Taken together, the mentioned polymorphisms might affect risk of GBM in Iranian population. Future studies are needed to elaborate the underlying mechanism.
Oral squamous cell carcinoma (OSCC), one of the most common types of head and neck squamous cell carcinoma (HNSCC), is characterized by high incidence and mortality. PVT1 is a long non-coding RNA (lncRNA) that plays an o...Oral squamous cell carcinoma (OSCC), one of the most common types of head and neck squamous cell carcinoma (HNSCC), is characterized by high incidence and mortality. PVT1 is a long non-coding RNA (lncRNA) that plays an oncogenic role in various cancer types. This study aims to reveal the role and underlying molecular mechanism of PVT1 in OSCC progression. The expression levels of PVT1, miR-7-5p, and CDKL1 mRNA were evaluated using qRT-PCR. Western blot and IHC analysis were conducted to determine the protein expression of CDKL1. The biological functions of PVT1, miR-7-5p, and CDKL1 in OSCC were investigated through CCK-8, transwell migration and invasion assays. In vivo experiments utilized a xenograft model to examine the impact of PVT1 on OSCC. Furthermore, the interaction among PVT1, miR-7-5p, and CDKL1 was explored using RNA pull down assay and luciferase reporter assays. We found that PVT1 enhanced cell proliferation, migration, and invasion by targeting CDKL1. In addition, PVT1 functions as a sponge to modulate miR-7-5p, thereby influencing the expression of CDKL1 and the progression of OSCC. In conclusion, this study illustrates that the "PVT1/miR-7-5p/CDKL1" pathway is capable of promoting the progression of OSCC and may serve as a promising target for developing treatment strategies for OSCC.
BACKGROUND: Low-dose spiral CT imaging has been employed for cancer diagnosis, but its sensitivity and specificity were unsatisfactory. MicroRNAs have been considered an approach for screening cancers, and the function o...BACKGROUND: Low-dose spiral CT imaging has been employed for cancer diagnosis, but its sensitivity and specificity were unsatisfactory. MicroRNAs have been considered an approach for screening cancers, and the function of miR-155-5p in lung cancer has been previously revealed. OBJECTIVES: This study assessed the diagnostic value of combining low-dose spiral CT with serum miR-155-5p in lung cancer aiming to explore a novel strategy to assist the clinical cancer diagnosis. METHODS: This study enrolled 115 lung cancer patients and 115 patients with benign lung diseases as control. All patients received low-dose spiral CT imaging, and serum miR-155-5p levels were analyzed by PCR. The diagnostic potential of miR-155-5p in lung cancer was evaluated by receiver operating curve (ROC), and its significance in evaluating the risk of lung cancer was evaluated by logistic regression analysis. The consistency of serum miR-155-5p and low-dose spiral CT imaging with pathological examination was assessed by the Kappa test. RESULTS: Reduced serum miR-155-5p indicated the risk of lung cancer in patients with benign lung diseases. Decreased serum miR-155-5p showed significant diagnostic value in early lung cancer and was significantly associated with disease severity. Low-dose spiral CT imaging showed significant diagnostic value in early lung cancer and showed middle consistency with pathological examination. Combining low-dose spiral CT imaging with serum miR-155-5p improved the diagnostic sensitivity and accuracy in early lung cancer, reduced the false positive rate, and showed better consistency with pathological examination. CONCLUSION: Serum miR-155-5p levels could assist the early detection of lung cancer by low-dose spiral CT examination.