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MiR-15b-5b Regulates the Proliferation of Prostate Cancer PC-3 Cells via Targeting LATS2
PURPOSE: In order to investigate the role of miR-15b-5b in the progression of prostate cancer. METHODS: We 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 tu...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7604262/ https://www.ncbi.nlm.nih.gov/pubmed/33149674 http://dx.doi.org/10.2147/CMAR.S266421 |
Sumario: | PURPOSE: In order to investigate the role of miR-15b-5b in the progression of prostate cancer. METHODS: We 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. RESULTS: MiR-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. CONCLUSION: The 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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