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LIN28B/IRS1 axis is targeted by miR‐30a‐5p and promotes tumor growth in colorectal cancer
Author(s) -
Tang Mei,
Zhou Jing,
You Lirui,
Cui Zhirong,
Zhang Hui
Publication year - 2020
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.29529
Subject(s) - irs1 , oncogene , gene silencing , cancer research , cell growth , biology , cancer , colorectal cancer , carcinogenesis , cell , microbiology and biotechnology , cell cycle , gene , genetics , endocrinology , insulin receptor , insulin , insulin resistance
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.