Circular RNA circWHSC1 facilitates colorectal cancer cell proliferation by targeting miR-130a-5p/zeb1 signaling in vitro and in vivo

环状 RNA circWHSC1 通过靶向 miR-130a-5p/zeb1 信号在体内和体外促进结直肠癌细胞增殖

阅读:6
作者:Lei Shi, Yuanshun Zhao, Xu Liu, Jingyao Qian, Xiao Yang, Wen Li

Abstract

Colorectal cancer is a prevalent cancer globally and has become a threaten of human health. Recently, circular RNAs (circRNAs) have been widely studied in the cancer area, and the function of circular RNA circWHSC1 has been identified in several cancers. However, the role of circWHSC1 in colorectal cancer remains elusive. In this study, we were interested in the effects of circWHSC1 on colorectal cancer progression. We found that level of circWHSC1 was elevated in colorectal cancer cells compared with normal colon epithelial cells. FISH assay further confirmed that circWHSC1 was mainly localized in cytoplasm. CircWHSC1 depletion repressed the viability of colorectal cancer cells. The colony formation number and Edu-positive colorectal cancer cells were inhibited by the depletion of circWHSC1, respectively. The knockdown of circWHSC1 promoted the apoptosis of colorectal cancer cells. The tumor growth of colorectal cancer cells in nude mice was attenuated by circWHSC1 silencing. Meanwhile, the invasion and migration ability of colorectal cancer cells was suppressed by circWHSC1 depletion. Mechanically, circWHSC1 targets miR-130a-5p to promote zeb1 expression in colorectal cancer cell. The depletion of circWHSC1 remarkably reduced the cell viability and Edu-positive colorectal cancer cells, and the miR-130a-5p inhibitor or zeb1 overexpression could restore the phenotypes. Furthermore, the tumor growth of colorectal cancer cells in nude mice was attenuated by circWHSC1 knockdown, while miR-130a-5p depletion or zeb1 overexpression reversed the effect in the model. Therefore, we concluded that Circular RNA circWHSC1 facilitated colorectal cancer cell proliferation by targeting miR-130a-5p/zeb1 signaling in vitro and in vivo.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。