ArticleCell death & disease2020
The miR-361-3p increases enzalutamide (Enz) sensitivity via targeting the ARv7 and MKNK2 to better suppress the Enz-resistant prostate cancer.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Circadian rhythm-related miR-6883-5p suppresses enzalutamide-resistant prostate cancer.Non-coding RNA research · 2026Article
- Molecular Mechanisms of Prostate Cancer Development in the Precision Medicine Era: A Comprehensive Review.Cancers · 2024Review
- MiR-125b targeted regulation of MKNK2 inhibits multiple myeloma proliferation and invasion.American journal of translational research · 2024Article
- LncRNA BBOX1-AS1 Contributes to the Progression of Esophageal Carcinoma by Targeting the miR-361-3p/COL5A1 Axis.Biochemical genetics · 2023Article
- The functional role of circular RNAs in the pathogenesis of retinoblastoma: a new potential biomarker and therapeutic target?Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Review
- Adaptation to Hypoxia May Promote Therapeutic Resistance to Androgen Receptor Inhibition in Triple-Negative Breast Cancer.International journal of molecular sciences · 2022Review
- Long noncoding RNA BBOX1-AS1 promotes the progression of gastric cancer by regulating the miR-361-3p/Mucin 13 signaling axis.Bioengineered · 2022Article
- Role of lncRNA MIAT/miR-361-3p/CCAR2 in prostate cancer cells.Open medicine (Warsaw, Poland) · 2022Article
- Regulation of Neuroendocrine-like Differentiation in Prostate Cancer by Non-Coding RNAs.Non-coding RNA · 2021Review
- Interaction between Non-Coding RNAs and Androgen Receptor with an Especial Focus on Prostate Cancer.Cells · 2021Review
- Identification of circ_0058357 as a regulator in non-small cell lung cancer cells resistant to cisplatin by miR-361-3p/ABCC1 axis.Thoracic cancer · 2021Article
- EIF4A3-induced circular RNA PRKAR1B promotes osteosarcoma progression by miR-361-3p-mediated induction of FZD4 expression.Cell death & disease · 2021Article
- Review
- Hsa_circ_0011385 knockdown represses cell proliferation in hepatocellular carcinoma.Cell death discovery · 2021Article
- Role of noncoding RNA in drug resistance of prostate cancer.Cell death & disease · 2021Review
- Androgen Receptor-Related Non-coding RNAs in Prostate Cancer.Frontiers in cell and developmental biology · 2021Review
- The Role of the SOX9/lncRNA ANXA2P2/miR-361-3p/SOX9 Regulatory Loop in Cervical Cancer Cell Growth and Resistance to Cisplatin.Frontiers in oncology · 2021Article
- Roles of Key Epigenetic Regulators in the Gene Transcription and Progression of Prostate Cancer.Frontiers in molecular biosciences · 2021Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
The androgen receptor splicing variant 7 (ARv7) that lacks the ligand-binding domain is increasingly considered as a key player leading to enzalutamide (Enz) resistance in patients with prostate cancer (PCa). However, the detailed mechanisms of how ARv7 expression is regulated and whether it also needs other factors to induce maximal Enz resistance remain unclear. Here, we identified a microRNA, miR-361-3p, whose expression is lower in patients with recurrent PCa, could function via binding to the 3'UTR of ARv7, but not the wild type of AR, to suppress its expression to increase the Enz sensitivity. Importantly, we found that miR-361-3p could also bind to the 3'UTR of MAP kinase-interacting serine/threonine kinase 2 (MKNK2) to suppress its expression to further increase the Enz sensitivity. In turn, the increased Enz can then function via a feedback mechanism through altering the HIF-2α/VEGFA signaling to suppress the expression of miR-361-3p under hypoxia conditions. Preclinical studies using an in vivo mouse model with orthotopically xenografted CWR22Rv1 cells demonstrated that combining the Enz with the small molecule miR-361-3p would result in better suppression of the Enz-resistant PCa tumor progression. Together, these preclinical studies demonstrate that miR-361-3p can function via suppressing the expression of ARv7 and MKNK2 to maximally increase the Enz sensitivity, and targeting these newly identified Enz/miR-361-3p/ARv7 and/or Enz/miR-361-3p/MKNK2 signals with small molecules may help in the development of novel therapies to better suppress the CRPC in patients that already have developed the Enz resistance.
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