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Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
07:49

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling

Published on: August 3, 2018

Transforming growth factor beta 1-induced delay of cell cycle progression and its association with growth-related

T A Kim1, A F Cutry, A J Kinniburgh

  • 1Department of Biochemistry, Roswell Park Cancer Institute, Buffalo, NY 14263.

Cancer Letters
|July 30, 1993
PubMed

Insights

Transforming growth factor beta (TGF-β) slows cell cycle progression and alters growth-related gene expression in fibroblasts. This study reveals TGF-β

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Cell cycle progression is regulated by growth factors like epidermal growth factor (EGF) and platelet-derived growth factor (PDGF).
  • Transforming growth factor beta (TGF-β) is known to influence cell growth and differentiation, but its precise role in cell cycle kinetics and gene expression requires further elucidation.

Purpose of the Study:

  • To investigate the effect of TGF-β on cell cycle progression in mouse fibroblasts.
  • To analyze the impact of TGF-β on the expression of immediate early genes (IEGs) and compare it with EGF and PDGF-BB.
  • To determine the involvement of PDGF-like proteins in TGF-β-induced DNA synthesis.

Main Methods:

  • Treatment of C3H 10T1/2 mouse fibroblasts with TGF-β, EGF, and PDGF-BB.
  • Measurement of cell cycle progression rates.
  • Quantification of mRNA levels for immediate early genes (c-myc, c-fos, c-jun, junB) and c-sis.
  • Inhibition studies using anti-PDGF-AB antibody.

Main Results:

  • TGF-β induced slower cell cycle progression compared to EGF or PDGF-BB.
  • TGF-β delayed the entry into S-phase induced by EGF or PDGF-BB.
  • TGF-β exhibited slower kinetics in inducing mRNA levels of immediate early genes (c-myc, c-fos, c-jun, junB) than EGF.
  • TGF-β induced c-sis gene expression, suggesting a potential role for PDGF-like proteins.
  • Anti-PDGF-AB antibody did not inhibit TGF-β-induced DNA synthesis.

Conclusions:

  • TGF-β delays cell cycle progression in fibroblasts.
  • The delay in cell cycle progression by TGF-β is linked to altered regulation of growth-related gene expression.
  • TGF-β's effects on cell cycle and gene expression are distinct from those of EGF and PDGF-BB, with limited involvement of PDGF-like pathways in its DNA synthesis induction.

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