STAT3-mediated transcription of Bcl-2, Mcl-1 and c-IAP2 prevents apoptosis in polyamine-depleted cells
作者： Sujoy Bhattacharya , Ramesh M. Ray , Leonard R. Johnson
DOI: 10.1042/BJ20050465
关键词: Cell culture 、 Apoptosis 、 Cell 、 Small interfering RNA 、 Inhibitor of apoptosis 、 STAT3 、 Biology 、 Tumor necrosis factor alpha 、 Molecular biology 、 STAT protein
摘要: Activation of STAT3 (signal transducer and activator transcription 3) plays a crucial role in cell survival proliferation. The aim the present study was to clarify signalling protection polyamine-depleted intestinal epithelial cells against TNF-α (tumour necrosis factor-α)-induced apoptosis. Polyamine depletion by DFMO (α-difluoromethylornithine) caused phosphorylation at Tyr-705 Ser-727. Phospho-Tyr-705 immunolocalized periphery nucleus, whereas phospho-Ser-727 predominantly detected nucleus cells. Sustained tyrosine residues observed after exposure TNF-α. Inhibition activation AG490 or cell-membrane-permeant inhibitory peptide (PpYLKTK; where pY represents phospho-Tyr) increased sensitivity Expression DN-STAT3 (dominant negative-STAT3) completely eliminated protective effect TNF-α-induced mRNA protein levels for Bcl-2, Mcl-1 (myeloid leukaemia-1) c-IAP2 (inhibitor apoptosis protein-2). Significantly higher Bcl-2 proteins were before 9 h treatment. decreased promoter activity. siRNA (small interfering RNA)-mediated inhibition induced caspase-3 PARP [poly(ADP-ribose) polymerase] cleavage These results suggest that response polyamine increases subsequent expression anti-apoptotic IAP family thereby promotes
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