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PI 3-kinase/Akt and STAT3 are required for the prevention of TGF-β-induced Hep3B cell apoptosis by autocrine motility factor/phosphoglucose isomerase

Authors
Journal
Cancer Letters
0304-3835
Publisher
Elsevier
Publication Date
Volume
290
Issue
2
Identifiers
DOI: 10.1016/j.canlet.2009.09.014
Keywords
  • Amf/Pgi
  • Tgf-β
  • Pi 3-Kinase
  • Akt
  • Stat3

Abstract

Abstract We established Hep3B cells stably-expressing wild-type and mutated AMF/PGI with differing enzymatic activities in order to investigate how AMF/PGI affects TGF-β-induced apoptosis, and demonstrated that AMF/PGI against TGF-β-induced apoptosis was correlated with its enzymatic activity. AMF/PGI did not alter TGF-β-receptor expression nor affect TGF-β-induced PAI-1 gene promoter or Smad3/4 activity. AMF/PGI induced PI 3-kinase activity, IRS and Akt phosphorylation, which can further regulate BAD phosphorylation. Constitutively-active p110 enhanced AMF/PGI-mediated anti-apoptosis activity, and dominant negative Akt alleviated anti-TGF-β-induced apoptosis. We also demonstrated that STAT3 is a weak anti-apoptotic agent but has an increased anti-apoptotic effect in cooperation with PI 3-kinase/Akt.

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