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Updated: Feb 12, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
10:37

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

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Identification of Epithelial-Mesenchymal Transition-related Target Genes Induced by the Mutation of Smad3 Linker

Sujin Park1, Kyung-Min Yang1, Yuna Park1,2

  • 1Precision Medicine Research Center, Advanced Institutes of Convergence Technology, Suwon, Korea.

Journal of Cancer Prevention
|April 10, 2018
PubMed
Abstract

Insights

Inhibiting Smad3 linker phosphorylation (Smad3-EPSM) enhances cancer cell motility and invasiveness. This study identifies GADD45B, CTGF, and JUNB as key genes involved in this process, offering potential therapeutic targets.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Metastasis

Background:

  • Smad3 linker phosphorylation is crucial for tumor progression and metastasis.
  • Previous work showed Smad3-EPSM mutation reduced tumor progression but increased lung metastasis in breast cancer.

Purpose of the Study:

  • To identify genes regulated by Smad3-EPSM using RNA-Sequencing.
  • To understand the role of Smad3 linker phosphorylation in cancer cell behavior.

Main Methods:

  • High-throughput RNA-Sequencing was performed on human prostate cancer cell lines infected with adenoviral Smad3-EPSM.
  • Gene expression profiles were analyzed in response to Smad3-EPSM.

Main Results:

  • Smad3-EPSM enhanced cell motility, invasiveness, and epithelial-mesenchymal transition marker gene expression (CDH2, SNAI1, ZEB1).
  • GADD45B, CTGF, and JUNB were identified as differentially regulated genes associated with Smad3-EPSM-induced cell motility and invasiveness.

Conclusions:

  • Inhibition of Smad3 linker phosphorylation may promote cancer cell motility and invasiveness.
  • Upregulation of GADD45B, CTGF, and JUNB is implicated in this process across various cancers.
Keywords:
Epithelial-mesenchymal transitionPancreatic cancerProstate cancerRNA sequence analysisSmad3

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