Role of MYC in Anchorage-Dependent Growth

Abstract

When deprived of adhesion normal cells are unable to proliferate; instead they arrest in G1 phase of the cell cycle. Unlike normal cells, transformed cells are able to by-pass this adhesion-mediated control of cell proliferation and grow in an anchorage-independent manner. Understanding the mechanism by which the extracellular matrix controls, progression through the G1 Phase of the cell cycle would give us insight into the cellular mechanism that accompany carcinogenesis. We have shown, here using a human mammary epithelial model, that the expression of the early growth control gene, c-Myc, is directly regulated by cell adhesion through a 1 integrin-dependent pathway, involving the PKC, c-Src family of kinase, and MAPK. When deprived of adhesion mammary epithelial cells are unable to progress into S phase upon EGF stimulation, and they arrest in early G1. This Anchorage-dependent block correlates with the down regulation of c-Myc mRNA and Protein.

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Document Details

Document Type
Technical Report
Publication Date
Sep 01, 2000
Accession Number
ADA391639

Entities

People

  • Christelle M. Benaud

Organizations

  • Georgetown University

Tags

DTIC Thesaurus Topics

  • Biomedical Research
  • Breast Cancer
  • Cell Biology
  • Cell Line
  • Cell Physiological Processes
  • Cells
  • Chemistry
  • Endothelial Cells
  • Epithelial Cells
  • Growth Factors
  • Molecular Dynamics
  • Mrna
  • Neoplasms
  • Peptide Growth Factors
  • Peptides
  • Proteins
  • Transcription Factors

Fields of Study

  • Biology

Readers

  • Breast cancer cell signaling and growth regulation.