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MicroRNA ‐92b acts as an oncogene by targeting PTEN / AKT in NSCLC
Author(s) -
Guo JiaHui,
Fang HaiYun,
Yang JunMei,
Liu ShanLing,
Yao QiangHua,
Fan YiJuan,
Zhao Mei,
Liu Feng,
Zhang QuanWu,
Gao FengHou
Publication year - 2020
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.3568
Subject(s) - pten , protein kinase b , cancer research , oncogene , gene knockdown , microrna , cell growth , pi3k/akt/mtor pathway , apoptosis , chemistry , biology , signal transduction , microbiology and biotechnology , cell cycle , gene , biochemistry
MicroRNAs can act as tumour suppressors or oncogenes by regulating cellular differentiation, proliferation and apoptosis, and the dysregulation of miRNA is involved in the occurrence and development of NSCLC. Here, we provided evidence that miR‐92b as an oncogene in NSCLC by targeting PTEN/AKT. We found that miR‐92b was up‐regulated in human NSCLC tissues and cell lines. MiR‐92b knockdown suppressed the NSCLC cells proliferation and migration in both in vivo and in vitro models. Conversely, miR‐92b overexpression induced an aggressive phenotype. Moreover, miR‐92b‐mediated regulation of NSCLC cell proliferation and migration depended on binding to PTEN mRNA, which then led to the degradation of PTEN and activation of the downstream AKT signalling pathway. Overall, this study revealed the oncogenic roles of miR‐92b in NSCLC by targeting PTEN/AKT, and provided novel insights for future treatments of NSCLC patients. Significance of the study MiR‐92b was up‐regulated in human NSCLC tissues and cell lines. Our study demonstrated that miR‐92b as an oncogene in NSCLC by targeting PTEN/AKT in both in vivo and in vitro models and provided novel insights for future treatments of NSCLC patients.