FAM83A signaling induces epithelial-mesenchymal transition by the PI3K/AKT/Snail pathway in NSCLC
Identifieur interne : 000820 ( Main/Exploration ); précédent : 000819; suivant : 000821FAM83A signaling induces epithelial-mesenchymal transition by the PI3K/AKT/Snail pathway in NSCLC
Auteurs : Fengrui Zhou [République populaire de Chine] ; Jianxiong Geng [République populaire de Chine] ; Shanqi Xu [République populaire de Chine] ; Qingwei Meng [République populaire de Chine] ; Kexin Chen [République populaire de Chine] ; Fang Liu [République populaire de Chine] ; Fang Yang [République populaire de Chine] ; Bo Pan [République populaire de Chine] ; Yan Yu [République populaire de Chine]Source :
- Aging (Albany NY) [ 1945-4589 ] ; 2019.
Abstract
Family with sequence similarity 83, member A (FAM83A), as a potential tumor promoter, was reported to contribute to the progression of several malignant tumors. However, the significance of FAM83A in invasion and metastasis of non-small cell lung cancer (NSCLC) remains largely unknown. In this study, we found that FAM83A expression was significantly increased in NSCLC tissues. High expression of FAM83A was positively associated with tumor metastasis and poor survival of NSCLC patients. Functional experiments revealed that FAM83A knockdown could suppress NSCLC cell migration and invasion both
Url:
DOI: 10.18632/aging.102163
PubMed: 31444970
PubMed Central: 6738414
Affiliations:
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<front><div type="abstract" xml:lang="en"><p>Family with sequence similarity 83, member A (FAM83A), as a potential tumor promoter, was reported to contribute to the progression of several malignant tumors. However, the significance of FAM83A in invasion and metastasis of non-small cell lung cancer (NSCLC) remains largely unknown. In this study, we found that FAM83A expression was significantly increased in NSCLC tissues. High expression of FAM83A was positively associated with tumor metastasis and poor survival of NSCLC patients. Functional experiments revealed that FAM83A knockdown could suppress NSCLC cell migration and invasion both <italic>in vivo</italic>
and <italic>in vitro</italic>
. While opposite results were observed in FAM83A-transfected cells. Mechanically, we found that FAM83A promoted NSCLC cell migration and invasion by inducing epithelial-mesenchymal transition (EMT) via PI3K/ATK/Snail signaling. Rescue experiment demonstrated that inhibition of either AKT or Snail could partially counteract the promoting effect of FAM83A overexpression in NSCLC metastasis. Taken together, our findings are the first time to demonstrate that increased expression of FAM83A in NSCLC was correlated with EMT and tumor metastasis, which may provide a novel therapeutic target in NSCLC treatment.</p>
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