Long non‑coding RNA RP11‑400N13.3 promotes the progression of colorectal cancer by regulating the miR‑4722‑3p/P2RY8 axis

长链非编码RNA RP11‑400N13.3通过调控miR‑4722‑3p/P2RY8轴促进结直肠癌进展

阅读:6
作者:Hongju Yang #, Qian Li #, Yanrui Wu, Jianlong Dong, Yaling Lao, Zheng Ding, Changyan Xiao, Jinxiao Fu, Song Bai

Abstract

Accumulating evidence has shown that long non‑coding RNAs (lncRNAs) play significant roles in the development and progression of many types of cancer including colorectal cancer. RP11‑400N13.3 is a novel lncRNA discovered recently and its biological function and underlying mechanism in colorectal cancer remain elusive. This study aimed to reveal the relationship between RP11‑400N13.3 and colorectal cancer. Our results demonstrated that the expression of RP11‑400N13.3 was significantly upregulated in both colorectal cancer tissues and cell lines as compared to normal adjacent tissues and normal colonic epithelial cells by RT‑qPCR, respectively. Upregulation of RP11‑400N13.3 was found to be correlated with a poor overall survival rate. Functional studies revealed that RP11‑400N13.3 facilitated the proliferation, migration, invasion and tumor growth of colorectal cancer cells while inhibiting the apoptosis of cancer cells in vitro and in vivo. We also observed that RP11‑400N13.3 serves as a sponge for miR‑4722‑3p, and that P2Y receptor family member 8 (P2RY8) was predicted to be a target of miR‑4722‑3p by bioinformatics analysis. Western blot assay indicated that the expression of P2RY8 was negatively or positively regulated by miR‑4722‑3p or RP11‑400N13.3. In addition, rescue experiments revealed that RP11‑400N13.3 promoted proliferation, migration and invasion by directly regulating the expression of miR‑4722‑3p and P2RY8. In conclusion, our results revealed that RP11‑400N13.3 promoted colorectal cancer progression via modulating the miR‑4722‑3p/P2RY8 axis, thus suggesting RP11‑400N13.3 as a potential therapeutic target for the treatment of colorectal cancer.

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。