ArticleCancer research2012
miR-23b represses proto-oncogene Src kinase and functions as methylation-silenced tumor suppressor with diagnostic and prognostic significance in prostate cancer.
Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 3 of them syntheses that pooled it.
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The trial behind it
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Who cites it
80 citing papers in PubMed, 3 syntheses or guidelines pooled it, 146 citations in OpenAlex.
- Downregulated miR-23b-3p expression acts as a predictor of hepatocellular carcinoma progression: A study based on public data and RT-qPCR verification.International journal of molecular medicine · 2018Pooled it
- The potential of microRNAs as human prostate cancer biomarkers: A meta-analysis of related studies.Journal of cellular biochemistry · 2018Pooled it
- Pooled it
- MicroRNA-23b: Roles, functions and mechanisms in tumor.Genes & diseases · 2026Review
- Age-Related Epigenetic Drift Shapes Coordinated microRNA Promoter Methylation and Expression in Prostate Cancer.Epigenomes · 2026Article
- miR-23b is a negative regulator of tumor suppressing PTPRG in colorectal cancer.Translational oncology · 2025Article
- A Brief Review of MicroRNA Profiling in Human Prostate Cancer Tissues and Plasma.Biomolecules · 2025Review
- RCOR1 is targeted by miR-23b-3p to modulate growth, colony formation, migration, and invasion of prostate cancer cells.International journal of clinical and experimental pathology · 2024Article
- MicroRNAs Can Influence Ovarian Cancer Progression by Dysregulating Integrin Activity.Cancers · 2023Review
- A transcriptome analysis of basal and stimulated VWF release from endothelial cells derived from patients with type 1 VWD.Blood advances · 2023Article
- Article
- Lactate promotes vascular smooth muscle cell switch to a synthetic phenotype by inhibiting miR-23b expression.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022Article
- Article
- Integrative Analysis and Experimental Validation Indicated That SNHG17 Is a Prognostic Marker in Prostate Cancer and a Modulator of the Tumor Microenvironment via a Competitive Endogenous RNA Regulatory Network.Oxidative medicine and cellular longevity · 2022Article
- Methylation and expression levels of microRNA-23b/-24-1/-27b, microRNA-30c-1/-30e, microRNA-301a and let-7g are dysregulated in clear cell renal cell carcinoma.Molecular biology reports · 2021Article
- Review
- Promotor Hypomethylation Mediated Upregulation of miR-23b-3p Targets PTEN to Promote Bronchial Epithelial-Mesenchymal Transition in Chronic Asthma.Frontiers in immunology · 2021Article
- Roles of Key Epigenetic Regulators in the Gene Transcription and Progression of Prostate Cancer.Frontiers in molecular biosciences · 2021Review
- MiRNA-671-5p Promotes prostate cancer development and metastasis by targeting NFIA/CRYAB axis.Cell death & disease · 2020Article
- Historical retrospective of theMolecular and clinical oncology · 2020Review
20 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
The miRNAs have great potential as biomarkers and therapeutic agents owing to their ability to control multiple genes and potential to influence cellular behavior. Here, we identified that miR-23b is a methylation-silenced tumor suppressor in prostate cancer. We showed that miR-23b expression is controlled by promoter methylation and has great promise as a diagnostic and prognostic biomarker in prostate cancer. High levels of miR-23b expression are positively correlated with higher overall and recurrence-free survival in patients with prostate cancer. Furthermore, we elucidated the tumor suppressor role of miR-23b using in vitro and in vivo models. We showed that proto-oncogene Src kinase and Akt are direct targets of miR-23b. Increased expression of miR-23b inhibited proliferation, colony formation, migration/invasion, and triggered G(0)-G(1) cell-cycle arrest and apoptosis in prostate cancer. Overexpression of miR-23b inhibited epithelial-to-mesenchymal transition (EMT) causing a decline in mesenchymal markers Vimentin and Snail and increasing the epithelial marker, E-cadherin. Depletion of Src by RNA interference conferred similar functional effects as that of miR-23b reconstitution. miR-23b expression caused a dramatic decrease in tumor growth in nude mice and attenuated Src expression in excised tumors compared with a control miR. These findings suggest that miR-23b is a methylation-silenced tumor suppressor that may be a useful biomarker in prostate cancer. Loss of miR-23b may confer proliferative advantage and promote prostate cancer migration and invasion, and reexpression of miR-23b may contribute to the epigenetic therapy for prostate cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.