ArticleCancer management and research2020
MiR-15b-5b Regulates the Proliferation of Prostate Cancer PC-3 Cells via Targeting LATS2.
Article in Cancer management and research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- MELK aggravates lung adenocarcinoma by regulating EZH2 ubiquitination and H3K27me3 histone methylation of LATS2.Journal of cellular and molecular medicine · 2024Article
- Treatment of Human Glioblastoma U251 Cells with Sulforaphane and a Peptide Nucleic Acid (PNA) Targeting miR-15b-5p: Synergistic Effects on Induction of Apoptosis.Molecules (Basel, Switzerland) · 2022Article
- Upregulated miRNAs on theFrontiers in genetics · 2022Article
- Review
- LINC01088 regulates the miR-95/LATS2 pathway through the ceRNA mechanism to inhibit the growth, invasion and migration of gastric cancer cells.International journal of immunopathology and pharmacologyArticle
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeIn order to investigate the role of miR-15b-5b in the progression of prostate cancer.
methodsWe employed RT-qPCR assay to analyze the transcriptional level of miR-15b-5b in cell lines including PC-3, prostate cancer tissues as well as normal prostate tissues. The protein level of large tumor suppressor factor 2 (LATS2) was detected by Western blot in similar specimens. Bioinformatic analysis was used to predict the targets of miR-15b-5p, and dual-luciferase assay was performed to confirm the relationship of miR-15b-5p with LATS2. Cell proliferation assay and colony formation assay were used to assess the effects of miR-15b-5b on the proliferation of PC-3 cells. Multivariate analysis was performed to identify factors associated with overall survival using the Cox proportional hazards model.
resultsMiR-15b-5b was up-regulated in prostate cancer tissues as well as cell lines, and increased expression of miR-15b-5b was highly correlated with the poor prognosis of patients with prostate cancer. Ectopic expression of miR-15b-5b promoted the proliferation of PC-3 cells. Reciprocally, silence of miR-15b-5b elicited opposite effects on cell proliferation. Mechanistically, we identified LATS2 as the target of miR-15b-5b, which in turn limited LATS2 expression in PC-3 cells. Furthermore, the stimulatory effects of miR-15b-5b on cell proliferation can be attenuated by overexpression of LATS2. Conversely, inhibition of LATS2 promoted the proliferation of PC-3 cells induced by miR-15b-5b. Our data thus demonstrate that dysregulation of miR-15b-5b exacerbates prostate cancer progression via suppression of LATS2.
conclusionThe identification of the oncogenic role of miR-15b-5b in prostate cancer thus proposes that miR-15b-5p might be a new therapeutic target for the treatment of prostate cancer.
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