BAG2 overexpression correlates with growth and poor prognosis of esophageal squamous cell carcinoma

Author:

Hong Ying-Cai1,Wang Zheng1,Peng Bin1,Xia Li-Gang2,Lin Lie-Wen2,Xu Zheng-Lei3

Affiliation:

1. Department of Thoracic Surgery, Shenzhen People's Hospital, 2nd Clinical Medical College of Jinan University, Shenzhen, Guangdong 518020, P.R.China

2. Department of Gastrointestinal Surgery, Shenzhen People's Hospital, 2nd Clinical Medical College of Jinan University, Shenzhen, Guangdong 518020, P.R.China

3. Department of Gastroenterology, Shenzhen People's Hospital, 2nd Clinical Medical College of Jinan University, Shenzhen, Guangdong 518020, P.R.China

Abstract

AbstractPrevious studies have suggested that Bcl2-associated athanogene 2 (BAG2) serves as a crucial regulator for tumorigenesis in multiple tumors. However, little is known about the effect of BAG2 on esophageal squamous cell carcinoma (ESCC). This study focused on investigating whether BAG2 functions as a cancer-promoting gene in ESCC. In this work, gene expression data and clinical information from the NCBI Gene Expression Omnibus (GEO), Oncomine and The Cancer Genome Atlas (TCGA) were collected and analyzed. Expression of BAG2 in ESCC was determined using quantitative reverse transcription polymerase chain reaction (qRT-PCR). BAG2 was knocked down using small interference RNA (si-RNA) approach. Cell proliferation, migration and invasion were assessed by Cell Counting Kit-8 (CCK-8) and transwell assays. Molecular mechanism was detected by western blotting assay. The expression of BAG2 both in ESCC tissues and cells was upregulated and overexpression was associated with worsened prognosis. BAG2 silencing inhibited ESCC cell proliferation, migration and invasion, which was regulated by the phosphatidylinositol-3-kinase (PI3K)/ protein kinase B (AKT) signaling pathway. These results reveal contributions of BAG2 as a predictor and potential therapeutic target in ESCC.

Publisher

Walter de Gruyter GmbH

Subject

General Agricultural and Biological Sciences,General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Neuroscience

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