PTEN公司
蛋白激酶B
癌症研究
癌基因
基因敲除
小RNA
细胞生长
PI3K/AKT/mTOR通路
细胞凋亡
化学
生物
信号转导
细胞生物学
细胞周期
基因
生物化学
作者
Jia‐Hui Guo,Fang Hai-yun,Junmei Yang,Shan‐Ling Liu,Qianghua Yao,Yi‐Juan Fan,Mei Zhao,Feng Liu,Quanwu Zhang,Feng‐Hou Gao
摘要
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.
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