Abstract
B-cell receptor-associated protein 31 (BAP31) has been shown to overexpress in a wide range type of cancers. The present study aims to investigate the role of BAP31 on migration in lung cancer. Results showed that the migration of BAP31 knockdown cells was weaken than the control cells. Applying TGFβ to treat BAP31 knockdown cells could reduce cell migration. The enhancement on proliferation by TGFβ treatment was downregulated after BAP31 knockdown. The cell death and G0/G1 phase arrest was increased in the cells with TGFβ and BAP31 siRNA treatment when compared with TGFβ treatment alone. Gene expression analysis showed that Bax/Bcl2, MLKL and LC3 was upregulated in the cells with combinatorial treatment of TGFβ and BAP31 siRNA. In addition, BAP31 was shown to regulate multiple signaling pathways, especially for Wnt signaling. It found that BAP31 knockdown cells treated with TGFβ decreased β-catenin cytosolic expression and nuclear localization. Wnt signaling activator BIO could restore the downregulation of proliferation by BAP31 knockdown. This finding suggested that BAP31 regulated cancer cell migration is possibly involved with cell death mechanisms and Wnt signaling.
Highlights
B-cell receptor-associated protein 31 (BAP31, or BCAP31), a polytopic integral membrane protein of the endoplasmic reticulum, has been primarily shown to regulate apoptosis by forming complex with Bcl2, Bcl-XL and procaspase-8 [1–3]
Transient expression of BAP31 over-expression plasmid was conducted in lung cancer cells A549, and Cell Counting Kit-8 (CCK-8) assay was performed in the cells received transfection for 24, 48, 72 and 96 hours (Figure S1)
TGFb is a key cytokine orchestrating epithelial-mesenchymal transition (EMT), and TGFb treatment would make epithelial cells change from cuboidal to an elongated spindle shape [21, 22]
Summary
B-cell receptor-associated protein 31 (BAP31, or BCAP31), a polytopic integral membrane protein of the endoplasmic reticulum, has been primarily shown to regulate apoptosis by forming complex with Bcl, Bcl-XL and procaspase-8 [1–3]. BAP31 has been recognized as a cancer/testis antigen [5]. BAP31 depletion has been shown to cell invasion and migration by modulating cytoskeleton assemblage [5]. BAP31 enhancing cell proliferation is found to be associated with serpin family E member 2 (SERPINE2) stabilization, and administration of antiBAP31 antibody could significantly prevent in vivo tumor growth [6]. BAP31 modulates migration and invasion via epithelial-mesenchymal transition (EMT) process [7]. Cell death was induced via regulating p27 proteasome degradation when applying a BAP31 intrabody in gastric cancer [8]. The function on cell death regulation of BAP31 in cancer cell migration has not yet been fully identified
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