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IGF-II enhances trichostatin A-induced TGFbeta1 and p21(Waf1,Cip1, sdi1) expression in Hep3B cells

S G Gray1, T Yakovleva, W Hartmann

  • 1Experimental Alcohol and Drug Addiction Research Section, Department of Clinical Neuroscience, Department of Clinical Neuroscience, Karolinska Institute, CMM, L8 01, Stockholm, S-171 76, Sweden.

Experimental Cell Research
|December 10, 1999
PubMed

Insights

Trichostatin A (TSA) induces cell growth arrest by upregulating cyclin dependent kinase inhibitors (CKIs) like p21. This study shows TSA affects IGF-II and TGFbeta1, and that IGF-II can modulate p21 induction.

Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Cell growth and division are regulated by cyclin-dependent kinases (CDKs) and their inhibitors (CKIs).
  • Trichostatin A (TSA) is known to induce the CKI p21, leading to cell growth arrest.
  • Transforming growth factor beta 1 (TGFbeta1) can also induce p21, and its latent form can be activated by M6P/IGF2R.

Purpose of the Study:

  • To investigate the effects of TSA on the IGF axis, CKIs (p21 and p27), and TGFbeta1 in Hep3B cells.
  • To determine how IGF-II and TGFbeta1 influence TSA-induced p21 expression.

Main Methods:

  • Treatment of Hep3B cells with Trichostatin A (TSA).
  • Analysis of IGF axis members, CKIs (p21, p27), TGFbeta1, and H19 gene expression.
  • Examination of the effects of adding IGF-II or TGFbeta1 to TSA-treated cells.

Main Results:

  • TSA treatment affected Insulin-like Growth Factor 2 (IGF2) and H19 gene expression.
  • TSA significantly enhanced TGFbeta1 expression and upregulated both p21 and p27.
  • IGF-II modulated TSA-induced p21 upregulation, while TGFbeta1 primarily affected its own expression.

Conclusions:

  • TSA-induced p21 expression and cell growth arrest involve multiple signaling pathways.
  • The interplay between IGF-II, TGFbeta1, and CKIs is crucial in mediating TSA's effects on cell cycle regulation.

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