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Updated: Jul 16, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
10:37

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

Evidence for involvement of phosphatidylcholine-phospholipase C and protein kinase C in transforming growth

J Halstead1, K Kemp, R A Ignotz

  • 1Department of Cell Biology, University of Massachusetts Medical Center, Worcester 01655, USA.

The Journal of Biological Chemistry
|June 9, 1995
PubMed

Insights

Transforming growth factor-beta (TGF-beta) signaling activates gene expression through phospholipase C and protein kinase C (PKC). Inhibiting these enzymes blocks TGF-beta

Area of Science:

  • Cellular signaling pathways
  • Molecular biology
  • Biochemistry

Background:

  • Transforming growth factor-beta (TGF-beta) is a key signaling molecule regulating cellular functions.
  • TGF-beta exerts its effects by binding to cell surface receptors with kinase domains.
  • Understanding TGF-beta's downstream signaling is crucial for comprehending its diverse cellular responses.

Purpose of the Study:

  • To investigate the role of phospholipase C and protein kinase C (PKC) in TGF-beta-induced gene transcription.
  • To identify the specific phospholipase C isoform involved in the TGF-beta signaling pathway.
  • To determine the impact of inhibiting PC-PLC and PKC on TGF-beta-mediated gene expression.

Main Methods:

  • Utilized the p3TP-Lux plasmid to measure TGF-beta-induced luciferase expression.
  • Employed PKC inhibitors (Staurosporin, Calphostin C) and a PC-PLC inhibitor (D609).
  • Assessed mRNA levels of endogenous genes (PAI-1, fibronectin) using quantitative methods.

Main Results:

  • Phospholipase C and PKC are integral to TGF-beta-induced transcription and luciferase expression.
  • Down-regulation or inhibition of PKC significantly blocks TGF-beta 1-induced gene transcription.
  • Inhibition of phosphatidylcholine-phospholipase C (PC-PLC) by D609, but not phosphatidylinositol-PLC by U73122, prevented TGF-beta 1-induced transcription.
  • TGF-beta-induced increases in PAI-1 and fibronectin mRNA levels were abrogated by PC-PLC and PKC inhibition.

Conclusions:

  • The study identifies a signaling pathway involving PC-PLC and PKC in TGF-beta-mediated gene expression.
  • These findings elucidate key molecular players in TGF-beta signal transduction.
  • The results suggest PC-PLC and PKC are essential for TGF-beta's transcriptional regulation of target genes.

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