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10.1016/j.yexcr.2017.04.016

http://scihub22266oqcxt.onion/10.1016/j.yexcr.2017.04.016
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C5514375!5514375!28433699
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suck abstract from ncbi

pmid28433699      Exp+Cell+Res 2017 ; 356 (1): 93-103
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  • EGFR-Mediated Apoptosis via STAT3 #MMPMID28433699
  • Jackson NM; Ceresa BP
  • Exp Cell Res 2017[Jul]; 356 (1): 93-103 PMID28433699show ga
  • The Epidermal Growth Factor Receptor (EGFR) is a cell surface receptor with primary implications in cell growth in both normal and malignant tissue. Paradoxically, cell lines that hyperexpress the EGFR have been documented to undergo receptor-mediated apoptosis. The underlying mechanism by which EGF-induced apoptosis occurs however remains inexplicit. In an attempt to identify this mechanism, we assessed downstream effectors of EGFR in MDA-MB-468 cells during conditions of EGF-induced apoptosis. The effector assessment revealed STAT3 as a potential mediator of EGF-induced apoptosis. Alternative strategies for activating STAT3, independent of EGFR stimulation, resulted in the induction of the apoptotic pathways. A reduction in STAT3 expression via RNAi resulted in a significant attenuation of EGF-induced PARP cleavage. Our findings support STAT3 as a positive mediator of EGF-induced apoptosis in MDA-MB-468 cells.
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