IRS1
癌基因
基因沉默
癌症研究
细胞生长
生物
癌症
结直肠癌
癌变
细胞
细胞生物学
细胞周期
基因
遗传学
内分泌学
胰岛素受体
胰岛素
胰岛素抵抗
作者
Mei Tang,Jing Zhou,Li-Rui You,Zhirong Cui,Hui Zhang
摘要
Abstract Insulin receptor substrate 1 (IRS1) is a potential oncogene that has been implicated in several malignant tumors. However, the regulatory mechanism of IRS1 remains to be investigated. The aim of our current study is to unveil the mechanism by which IRS1 exerts functions in tumorigenesis of colorectal cancer (CRC). The expression level of IRS1 was found to be higher in CRC cells in comparison with the normal cell. To determine the role of IRS1 in regulating CRC cellular processes, loss‐of‐function assays were designed and carried out in two CRC cell lines. Both in vitro and in vivo functional assays indicated that silencing of IRS1 suppressed CRC cell survival. Based on bioinformatics prediction and mechanism experiments, IRS1 was identified as a downstream target of miR‐30a‐5p. Furthermore, RNA‐binding protein lin‐28 homolog B (LIN28B) was determined to be a stabilizer of IRS1 messenger RNA. More importantly, LIN28B also acted as a target of miR‐30a‐5p.Through rescue assays, we proved that LIN28B‐stablized IRS1 mediated miR‐30a‐5p‐mediated CRC cell growth. In conclusion, this study revealed that LIN28B and LIN28B‐stablized IRS1 promoted CRC cell growth by cooperating with miR‐30a‐5p.
科研通智能强力驱动
Strongly Powered by AbleSci AI