期刊
CANCER RESEARCH
卷 72, 期 13, 页码 3393-3404出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-11-3864
关键词
-
类别
资金
- NIH [R01-ES015888, R21-CA150009]
- Department of Defense [W81XWH-08-1-0472, W81XWH-11-1-0331, W81XWH-10-1-0194]
- CPRIT [RP120380]
- MD Anderson Cancer Center Bridge fund
- Center for Cancer Epigenetics
- Laura and John Arnold Foundation RNA Center
- [CCSG-5 P30 CA016672]
- [ES007784]
MiRNAs regulate cancer cells, but their potential effects on cancer stem/progenitor cells are still being explored. In this study, we used quantitative real-time-PCR to define miRNA expression patterns in various stem/progenitor cell populations in prostate cancer, including CD44(+), CD133(+), integrin alpha 2 beta 1+, and side population cells. We identified distinct and common patterns in these different tumorigenic cell subsets. Multiple tumor-suppressive miRNAs were downregulated coordinately in several prostate cancer stem/progenitor cell populations, namely, miR-34a, let-7b, miR-106a, and miR-141, whereas miR-301 and miR-452 were commonly overexpressed. The let-7 overexpression inhibited prostate cancer cell proliferation and clonal expansion in vitro and tumor regeneration in vivo. In addition, let-7 and miR-34a exerted differential inhibitory effects in prostate cancer cells, with miR-34a inducing G(1) phase cell-cycle arrest accompanied by cell senescence and let-7 inducing G(2)-M phase cell-cycle arrest without senescence. Taken together, our findings define distinct miRNA expression patterns that coordinately regulate the tumorigenicity of prostate cancer cells. Cancer Res; 72(13); 3393-404. (C) 2012 AACR.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据