ArticleCancer biology & therapy2020
MiR-133a-5p inhibits androgen receptor (AR)-induced proliferation in prostate cancer cells via targeting FUsed in Sarcoma (FUS) and AR.
Article in Cancer biology & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 26 citations in OpenAlex.
- Review
- Regulatory roles of microRNAs in signaling pathways and their biomarker potential in prostate cancer.Cancer cell international · 2026Review
- Unravelling therapeutic resistance: role of cancer stem cell and microRNA in metastatic prostate cancer.Frontiers in molecular biosciences · 2026Review
- MiR-133a-5p Facilitates Cuproptosis in Hepatocellular Carcinoma Through Targeting of ATP7B.Journal of inflammation research · 2025Article
- Recent progress in microRNA research for prostate cancer.Discover oncology · 2024Review
- Manzamine A reduces androgen receptor transcription and synthesis by blocking E2F8-DNA interactions and effectively inhibits prostate tumor growth in mice.Molecular oncology · 2024Article
- Epigenetics in the formation of pathological aggregates in amyotrophic lateral sclerosis.Frontiers in molecular neuroscience · 2024Review
- Luteolin inhibits A549 cells proliferation and migration by down-regulating androgen receptors.European journal of medical research · 2023Article
- Article
- Deregulated microRNAs Involved in Prostate Cancer Aggressiveness and Treatment Resistance Mechanisms.Cancers · 2023Review
- Comparative miRNA expression profile analysis of porcine ovarian follicles: new insights into the initiation mechanism of follicular atresia.Frontiers in genetics · 2023Article
- Long non-coding RNA XIST promotes the malignant features of oral squamous cell carcinoma (OSCC) cells through regulating miR-133a-5p/VEGFB.Histology and histopathology · 2023Article
- Cypermethrin inhibits proliferation of Sertoli cells through AR involving DAB2IP/PI3K/AKT signaling pathway in vitro.Toxicology research · 2022Article
- The Role of Androgen Receptor and microRNA Interactions in Androgen-Dependent Diseases.International journal of molecular sciences · 2022Review
- miR-133a-5p Inhibits Glioma Cell Proliferation by Regulating IGFBP3.Journal of oncology · 2022Article
- Interaction between Non-Coding RNAs and Androgen Receptor with an Especial Focus on Prostate Cancer.Cells · 2021Review
- Long Non-coding RNA LINC01503 Promotes Gastric Cardia Adenocarcinoma Progression via miR-133a-5p/VIM Axis and EMT Process.Digestive diseases and sciences · 2021Article
- miR-130a-3p promotes cell proliferation and invasion by targeting estrogen receptor α and androgen receptor in cervical cancer.Experimental and therapeutic medicine · 2021Article
- LncRNA FER1L4 Promotes Oral Squamous Cell Carcinoma Progression via Targeting miR-133a-5p/Prx1 Axis.OncoTargets and therapy · 2021Article
- Emerging roles of MiR-133a in human cancers.Journal of Cancer · 2021Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Androgens and androgen receptors are vital factors involved in prostate cancer progression, and androgen ablation therapies are commonly employed to treat advanced prostate cancer. Previously, FUsed in Sarcoma (FUS) was identified as an AR-interacting protein that enhances AR transcriptional activity. In the present study, we attempted to identify miRNAs that might target both FUS and AR to inhibit FUS and AR expression. Based on TCGA data and the online tools UALCAN, Kaplan Meier-plotter (KMplot), LncTar and miRWalk prediction, miR-133a-5p was selected. MiR-133a-5p expression was significantly downregulated in prostate cancer, and low miR-133a-5p expression was correlated with low survival probability. As predicted by LncTar and miRWalk, miR-133a-5p could bind to the 3'UTR of FUS and AR to inhibit their expression. MiR-133a-5p overexpression significantly suppressed the cell viability of the AR-positive prostate cancer cell lines VCaP and LNCaP, inhibited the expression of FUS, AR, as well as AR downstream targets IGF1R and EGFR. More importantly, miR-133a inhibition increased cancer cell proliferation as well as the expression of AR and AR downstream factors, while FUS knockdown exerted an opposite effect; the effect of miR-133a on cancer cell proliferation and AR could be significantly reversed by FUS knockdown. Moreover, IGF1R and EGFR knockdown reversed the effect of the miR-133a-5p inhibition. In summary, miR-133a-5p inhibits AR-positive prostate cancer cell proliferation by targeting FUS/AR, thus improving the resistance of prostate cancer to androgen ablation therapies, which requires further
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