Progesterone Regulation of Insulin Receptor Substrates Mediates Focal Adhesion Formation in Breast Cancer Cells

Abstract

How progesterone and IGF signaling pathways cross-talk with each other to regulate breast cancer progression remains a critical question. In this study, it was found that progesterone enhances IGF-induced cell motility using PR-B-transfected C4-12 cells. To assess whether the progesterone effect is via regulation of IRS-l/2 expression and activation, I performed RT-PCR and western blot analysis. It was found that IRS-2 was sharply up-regulated by progestins through transcriptional mechanisms in MCF-7, T47D, ZR75, and especially in PR-B C4-12 cells while IRS- 1 was not. This indicates that IRS-1 and IRS-2 are distinctively regulated by progestins. Moreover, IRS-2 and its downstream signaling elicited by IGF-I were enhanced by progesterone, which was shown by immunoprecipitation. These data, together with previous findings that IRS-2 is activated by integrins, provide a clue that IRS-2 may be involved in progestin increase of IGF-induced cell motility.

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Document Details

Document Type
Technical Report
Publication Date
Jul 01, 2003
Accession Number
ADA418730

Entities

People

  • Adrian Lee
  • Xiaojang Cui

Organizations

  • Baylor University

Tags

DTIC Thesaurus Topics

  • Anti-Bacterial Agents
  • Biological Sciences
  • Biotechnology
  • Breast Cancer
  • Cell Membrane Structures
  • Cell Movement
  • Cell Physiological Processes
  • Cells
  • Chemistry
  • Gene Expression
  • Genetics
  • Indicator Dyes
  • Molecular Biology
  • Neoplasms
  • Peptide Growth Factors
  • Peptides
  • Proteins

Fields of Study

  • Biology

Readers

  • Breast cancer cell signaling and growth regulation.