Critical Contribution of Ral GTPases to Growth and Survival of Breast Cancer

Abstract

We have previously identified the Ras-like GTpases, RalA and RalB as linchpin modulators of human tumor cell proliferation and survival. Using RNAi-mediated loss-of-function analysis, we find that RalA is critical for anchorage-independent growth whereas RalB is required for tumor cell survival. The collaboration of these isoform-specific contributions generates a minimal oncogenic platform, which results in aberrant proliferation coupled with suppression of apoptosis. We have begun to characterize the molecular basis of the collaborative contributions of RalA and RalB to cell regulation. These studies have surprisingly revealed that RalB and Sec5 are mediating tumor cell survival whereas RalA and STAT3 contribute to anchorage-independent proliferation. Understanding how the regulation occurs will be the focus of my future work.

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Document Details

Document Type
Technical Report
Publication Date
Apr 01, 2005
Accession Number
ADA435549

Entities

People

  • Yuchen Chien

Organizations

  • University of Texas Southwestern Medical Center

Tags

DTIC Thesaurus Topics

  • Apoptosis
  • Breast Cancer
  • Cell Line
  • Cell Physiological Processes
  • Cells
  • Cytoskeleton
  • Epithelial Cells
  • Instructions
  • Modulators
  • Platforms
  • Programmed Cell Death
  • Proteins
  • Regulations
  • Tumor Cell Line

Readers

  • Molecular Biology and Genetics