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miR‐377‐3p drives malignancy characteristics via upregulating GSK‐3β expression and activating NF‐κB pathway in hCRC cells
Author(s) -
Liu WeiYing,
Yang Zhen,
Sun Qi,
Yang Xi,
Hu Yang,
Xie Hong,
Gao HuiJie,
Guo LiMing,
Yi JianYing,
Liu Min,
Tang Hua
Publication year - 2018
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.26374
Subject(s) - downregulation and upregulation , carcinogenesis , cancer research , gene knockdown , oncogene , microrna , gsk 3 , nf κb , epithelial–mesenchymal transition , chemistry , apoptosis , biology , signal transduction , cancer , microbiology and biotechnology , cell cycle , gene , genetics , biochemistry
MicroRNA (miRNA) dysregulation has been associated with carcinogenesis in many cancers, including human colorectal cancer (hCRC). However, the effect and mechanism of miR‐377‐3p on CRC remains elusive. Herein, we first found that miR‐377‐3p was upregulated in CRC tissues and promoted tumorigenic activity by accelerating the G 1 ‐S phase transition, promoting cell proliferation and epithelial‐mesenchymal transition (EMT) while repressing apoptosis in CRC cells. Glycogen synthase kinase‐3β (GSK‐3β) was a direct target of miR‐377‐3p, and upregulated by miR‐377‐3p. Knockdown of GSK‐3β partly rescued miR‐377‐3p‐mediated malignancy characteristics. Most importantly, we showed that miR‐377‐3p promoted carcinogenesis by activating NF‐κB pathway. Taken together, our results first reported that miR‐377‐3p functions as an oncogene and promotes carcinogenesis via upregulating GSK‐3β expression and activating NF‐κB pathway in hCRC cells.