Bag3 promotes resistance to apoptosis through Bcl-2 family members in non-small cell lung cancer
Author(s) -
Qiang Lü
Publication year - 2011
Publication title -
oncology reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.094
H-Index - 96
eISSN - 1791-2431
pISSN - 1021-335X
DOI - 10.3892/or.2011.1486
Subject(s) - apoptosis , cancer research , bag3 , gene silencing , biology , oncogene , lung cancer , cell , cell culture , cell cycle , programmed cell death , oncology , medicine , gene , genetics
In non-small cell lung cancer (NSCLC) certain molecular characteristics,which are related to molecular alterations have been investigated. These are responsiblefor both the initiation and maintenance of the malignancy in lung cancer. Theaim of this study was to evaluate the influence of Bag3 (Bcl-2 associated athanogene3) in the regulation of apoptosis on NSCLC. Bag3 and Hsp70 expression were examinedby immunohistochemistry to confirm their potential roles in the prevalence ofNSCLC. We also established human normal bronchial epithelial cells and HOP-62cell line as the model to analyze cell apoptosis and the expression of Hsp70,Bcl-XL and Bcl-2, which were affected by Bag3. In this study, we found that Bag3and Hsp70 are highly expressed in few tissues and cell lines of NSCLC. Bag3 inhibitsapoptosis in human normal bronchial epithelial cell lines and sustain the survivalof NSCLC cells. Bag3, Hsp70, Bcl-XL and Bcl-2 are up-regulated in NSCLC cell lines.At the same time, the silencing of Bag3 results in diminishing protein levelsof Bcl-XL and Bcl-2. The results of immunoprecipitation identified that Bag3 couldinteract with Hsp70, Bcl-XL and Bcl-2 NSCLC cells directly or indirectly. We concludethat NSCLC cells were protected from apoptosis through increasing Bag3 expressionand consequently promoted the expression of Bcl-XL and Bcl-2.
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