Wnt信号通路
细胞周期
细胞凋亡
癌症研究
细胞生长
前列腺癌
生物
小RNA
连环素
癌细胞
癌症
细胞生物学
化学
信号转导
生物化学
遗传学
基因
作者
J. C. Li,F. Liu,Gen Zhang,Wei Bai,W. S. Cheng,Y. Zhang,Toshio Seki
出处
期刊:PubMed
日期:2017-06-01
卷期号:21 (11): 2586-2595
被引量:13
摘要
Prostate cancer (PCa) is the second leading contributor to male malignancy-associated death in developed countries. The study aimed to evaluate the effects of lncRNA625/miR-432 on the prostate cancer cells and the underlying molecular mechanism.The cell proliferation was detected using the MTT and colony formation, and cells apoptosis and cell cycle were analyzed with the flow cytometry. Luciferase reporter assay was carried out to detect the correlation between miR-432 and TRIM29 and PYGO2. Besides, reverse transcription-PCR and Western blot were performed to detect the mRNA and protein levels in prostate tissues and PC3 cells.lncRNA625 and miR-432 levels were consistently reduced in the PCa tissues compared with the healthy control and lncRNA625 levels significantly affect the miR-432 expression in PC3 cells, indicating that miR-432 is a direct target of lncRNA625. Besides, lncRNA625 overexpression could inhibit the cancer cells growth, arresting cell cycle progression at the G1/S phase, and significantly induce apoptosis of PC3 cells, but reversed by the miR-432 inhibitor. Most importantly, we further found that miR-432 could deactivate Wnt/β-catenin pathway via suppressing TRIM29 and PYGO2 directly.lncRNA625 could functionally inhibit PC3 cells proliferation and promote cells apoptosis through regulating the Wnt/β-catenin pathway by targeting miR-432.
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