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Growth suppression induced by Notch1 activation involves Wnt-beta-catenin down-regulation in human tongue carcinoma

Li Duan1, Jun Yao, Xinxing Wu

  • 1Key Laboratory for Oral Biomedical Engineering of Ministry of Education, School and Hospital of Stomatology, Wuhan University, Wuhan, Hubei 430079, People's Republic of China.

Biology of the Cell
|April 13, 2006
PubMed
Abstract

Insights

Notch1 signaling inhibits human tongue cancer growth by inducing cell cycle arrest and apoptosis. This pathway may suppress tumors by down-regulating beta-catenin, a key component of Wnt signaling.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Notch1 signaling is implicated in various cancers.
  • Its specific role in human tongue squamous cell carcinoma is not well understood.

Purpose of the Study:

  • To investigate the function of Notch1 signaling in human tongue cancer.
  • To explore the underlying molecular mechanisms of Notch1's effect on tongue cancer cells.

Main Methods:

  • Stable transfection of Tca8113 human tongue cancer cells with exogenous ICN (intracellular fragment of Notch) to over-express active Notch1.
  • In vitro and in vivo studies to assess tumor growth.
  • Analysis of cell cycle progression, apoptosis, and expression levels of key proteins including beta-catenin, p21(WAF1/CIP1), p53, Skp2, and Bcl-2.

Main Results:

  • Constitutive over-expression of active Notch1 suppressed Tca8113 cell growth both in vitro and in vivo.
  • Active Notch1 induced G(0)-G(1) cell cycle arrest and apoptosis.
  • Down-regulation of beta-catenin, p21(WAF1/CIP1) and p53 expression increased, while Skp2 and Bcl-2 expression decreased.

Conclusions:

  • Notch1 exhibits anti-proliferative effects on human tongue cancer cells.
  • Down-regulation of Wnt/beta-catenin signaling is a potential mechanism by which Notch1 induces apoptosis and cell cycle arrest in this cancer type.

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