MiR-29a suppresses prostate cell proliferation and induces apoptosis via KDM5B protein regulation.
MiR-29a suppresses prostate cell proliferation and induces apoptosis via KDM5B protein regulation.
复制标题
MiR-29a 通过 KDM5B 蛋白调节抑制前列腺细胞增殖并诱导细胞凋亡。
DOI：
--
复制
发表时间：
2015-04
影响因子：
0.1
通讯作者：
Li, Yao
中科院分区：
文献类型：
--
作者：
Huang, Wenhua;Huang, Shengsong;Wu, Denglong;Li, Yao
Small regulatory RNAs, known as microRNAs, regulate gene expression at the post-transcriptional level; such as protein translation inhibition or mRNA degradation. Altered miRNA expressions have been implicated in various cancers. In present studies, it was demonstrated that microRNA-29a (miR-29a) expressions were significantly lower in prostate cancer (PCa) patient samples, but the role of microRNA-29s in PCa remains unclear. KDM5B was highly expressed in PCa cancer cells. Bioinformatics analysis revealed a conserved target site for miR-29a in the 3-untranslated region (UTR) of KDM5B. Gain-of-function studies using mature miR-29a were performed to investigate cell proliferation and apoptosis in two PCa cell lines (LNCaP and PC-3). We utilized gene expression analysis and in silico database analysis to identify miR-29a-mediated molecular pathways and targets. We showed that miR-29a significantly suppressed the activity of a lucifarice reporter containing KDM5B-3'UTR, which was not observed in cells transfected with mutated KDM5B-3'UTR. Gene expression data demonstrated that KDM5B expression was lower in noncancerous prostatic cell WPMY-1 than in the four PCa cell lines (LNCaP, 22RV1, PC-3 and DU145). Moreover, the enforced expression of miR-29a in PC-3 and LNCaP cells inhibited proliferation, and induced apoptosis by repressing the expression of KDM5B. This study revealed that the aberrant expression of miR-29a in PCa cells regulated KDM5B expression levels associated with tumor dissemination. These findings may be utilized in developing novel therapeutic tools for PCa.
登录
查看更多内容
DOI：
10.1891/9780826121646.0002
发表时间：
2018-09
期刊：
Cancer Rehabilitation
影响因子：
--
作者：
K. Miller;R. Siegel;R. Khan;A. Jemal
通讯作者：
K. Miller;R. Siegel;R. Khan;A. Jemal
影响因子：
8
作者：
Noonan, E. J.;Place, R. F.;Dahiya, R.
通讯作者：
Dahiya, R.
DOI：
10.1016/j.bbrc.2009.03.077
发表时间：
2009-06-05
影响因子：
3.1
作者：
Li, Tao;Li, Dong;Huang, Yiran
通讯作者：
Huang, Yiran
DOI：
10.1126/science.1189862
发表时间：
2010-06-18
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Rayner KJ;Suárez Y;Dávalos A;Parathath S;Fitzgerald ML;Tamehiro N;Fisher EA;Moore KJ;Fernández-Hernando C
通讯作者：
Fernández-Hernando C
影响因子：
11.2
作者：
Iorio, MV;Ferracin, M;Croce, CM
通讯作者：
Croce, CM