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FAM83A is amplified and promotes tumorigenicity in non-small cell lung cancer via ERK and PI3K/Akt/mTOR pathways by Hu, Haiyang; Wang, Fajiu; Wang, Muyun; Liu, Yuanyuan; Wu, Han; Chen, Xi; Lin, Qiang is a Medicine article available to read on EtoBox.

What is FAM83A is amplified and promotes tumorigenicity in non-small cell lung cancer via ERK and PI3K/Akt/mTOR pathways about?

Family with sequence similarity 83A (FAM83A) is a newly-found over-expressed oncogene in several types of cancers and associates with poor prognosis. However, the role that FAM83A may play in the carcinogenesis of non-small cell lung cancer (NSCLC) still needs to be defined. The present study aimed to investigate the function of FAM83A in NSCLC progression and to investigate the possible mechanism. Analysis of Gene Expression Omnibus (GEO) database and rt-PCR showed up-regulated expression of FAM83A in NSCLC. GEO and the Cancer Genome Atlas (TCGA) data analysis revealed that high expression level of FAM83A in NSCLC was associated with poor prognosis. __In vitro__ experiments showed that depleting FAM83A by siRNA/shRNA significantly inhibited cell proliferation and induced cell apoptosis. Cell motility was also retarded after silencing FAM83A, as demonstrated by Transwell assay. FAM83A depletion in A549 cells also inhibited subcutaneous tumor growth and lung metastasis __in vivo__. Western blotting showed that silencing FAM83A decreased the phosphorylation of ERK and PI3K/Akt/mTOR. On the other hand, overexpressing FAM83A __in vitro__ enhanced cell proliferation and invasiveness, wh

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Author
Hu, Haiyang; Wang, Fajiu; Wang, Muyun; Liu, Yuanyuan; Wu, Han; Chen, Xi; Lin, Qiang
Publisher
Ivyspring International Publisher; Blue Haven NSW: Ivyspring International, 2004- (ISSN 1449-1907)
Published
2020
Language
EN
Field
Medicine (Life Sciences)

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