ArticleJournal of cellular and molecular medicine2020
MiR-129-5p promotes docetaxel resistance in prostate cancer by down-regulating CAMK2N1 expression.
Article in Journal of cellular and molecular medicine, 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, 36 citations in OpenAlex.
- A role for astrocytic miR-129-5p in frontotemporal dementia.Translational psychiatry · 2025Article
- Overexpression of miR-328-3p Inhibits Epithelial-Mesenchymal Transition in Prostate Cancer by Downregulating PFN1.Applied biochemistry and biotechnology · 2025Article
- Review
- LncRNA PITPNA-AS1 mediates the diagnostic potential of miR-129-5p in prostate cancer.BMC urology · 2024Article
- LncRNA RPLP0P2 Promotes Colorectal Cancer Proliferation and Invasion via the miR-129-5p/Zinc Finger and BTB Domain-Containing 20 Axis.Biochemical genetics · 2024Article
- Molecular panorama of therapy resistance in prostate cancer: a pre-clinical and bioinformatics analysis for clinical translation.Cancer metastasis reviews · 2024Review
- The value of a panel of circulating microRNAs in screening prostate cancer.Translational cancer research · 2024Article
- A serum panel of three microRNAs may serve as possible biomarkers for kidney renal clear cell carcinoma.Cancer cell international · 2024Article
- Non-Coding RNAs and the Development of Chemoresistance to Docetaxel in Prostate Cancer: Regulatory Interactions and Approaches Based on Machine Learning Methods.Life (Basel, Switzerland) · 2023Review
- Regulatory roles of ferroptosis-related non-coding RNAs and their research progress in urological malignancies.Frontiers in genetics · 2023Review
- The circSPON2/miR-331-3p axis regulates PRMT5, an epigenetic regulator of CAMK2N1 transcription and prostate cancer progression.Molecular cancer · 2022Article
- Circular RNA coiled-coil domain containing 66 regulates malignant development of papillary thyroid carcinoma by upregulating La ribonucleoprotein 1Bioengineered · 2022Article
- E2F transcription factor 2-activated DLEU2 contributes to prostate tumorigenesis by upregulating serum and glucocorticoid-induced protein kinase 1.Cell death & disease · 2022Article
- LncRNA RP11-89 facilitates tumorigenesis and ferroptosis resistance through PROM2-activated iron export by sponging miR-129-5p in bladder cancer.Cell death & disease · 2021Article
- Article
- Expression and regulatory network of miRNAs in head and neck squamous cell carcinoma.Translational cancer research · 2020Article
- MiR-129-5p promotes docetaxel resistance in prostate cancer by down-regulating CAMK2N1 expression.Journal of cellular and molecular medicine · 2020Article
- Clinical significance and potential mechanisms ofOpen medicine (Warsaw, Poland) · 2020Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study focuses on the effect of miR-129-5p on docetaxel-resistant (DR) prostate cancer (PCa) cells invasion, migration and apoptosis. In our study, the expression of CAMK2N1 was assessed by qRT-PCR in PCa patient tissues and cell lines including PC-3 and PC-3-DR. Cells transfected with miR-129-5p mimics, inhibitor, CAMK2N1 or negative controls (NC) were used to interrogate their effects on DR cell invasions, migrations and apoptosis during docetaxel (DTX) treatments. The apoptosis rate of the PCa cells was validated by flow cytometry. Relationships between miR-129-5p and CAMK2N1 levels were identified by qRT-PCR and dual-luciferase reporter assay. CAMK2N1 was found to be down-expressed in DR PCa tissue sample, and low levels of CAMK2N1 were correlated with high docetaxel resistance and clinical prediction of poor survival. CAMK2N1 levels were decreased in DR PCa cells treated with DXT. We further explored that up-regulation of miR-129-5p could promote DR PCa cells viability, invasion and migration but demote apoptosis. Involved molecular mechanism studies revealed that miR-129-5p reduced downstream CAMK2N1 expression to further impact on chemoresistance to docetaxel of PCa cells, indicating its vital role in PCa docetaxel resistance. Our findings revealed that miR-129-5p contributed to the resistance of PC-3-DR cells to docetaxel through suppressing CAMK2N1 expression, and thus targeting miR-129-5p may provide a novel therapeutic approach in sensitizing PCa to future docetaxel treatment.
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