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  • Title: Involvement of ERK, Bcl-2 family and caspase 3 in recombinant human activin A-induced apoptosis in A549.
    Author: Wang B, Feng Y, Song X, Liu Q, Ning Y, Ou X, Yang J, Zhang X, Wen F.
    Journal: Toxicology; 2009 Apr 28; 258(2-3):176-83. PubMed ID: 19428937.
    Abstract:
    BACKGROUND: Activins are members of the transforming growth factor-beta (TGF-beta) superfamily. Previous studies have shown that activin A may have a central role in regulating both apoptosis and proliferation. However, direct studies of recombination human activin A on human NSCLC A549 cells have not yet been reported. The purpose of this study was to investigate whether activin A could induce apoptosis in A549 cells and the possible mechanisms via which it worked. METHODS: Cellular apoptosis induced by activin A was detected by TUNEL assay and the levels of protein expression were detected by western blot. RESULTS: Recombination human activin A induced apoptosis in human NSCLC A549 cells in a concentrate-dependent manner. Activin A-induced A549 apoptosis was accompanied by the up-regulation of Bax, Bad and Bcl-Xs and down-regulation of Bcl-2. Moreover, activin A treatment increased the expression of its typeII receptors, activated ERK and caspase 3 in A549. These results clearly demonstrate that the induction of apoptosis by activin-A involves multiple cellular/molecular pathways and strongly suggest that pro- and anti-apoptotic Bcl-2 family proteins and caspase 3 participate in activin A-induced apoptotic process in A549 cells. On the other hand, activin A treatment had little effect on primary human small airway epithelial cells (SAECs). CONCLUSION: Recombination human activin A induced apoptosis in A549 cells, at least partially, through ERK and mitochondrial pathway. The result that activin A did not affect the normal SAEC revealed activin A might be considered as a potential anticancer agent and worthy of further studies.
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