Role of ei24/PIG8, A Putative Pro-Apoptotic Tumor Suppressor, in Breast Cancer Development and Resistance to Drug Therapy

Abstract

EI24/PIG8 is regulated by p53 in response to genotoxic damage and was shown to be genetically inactivated in aggressive breast cancers with frequent loss-of-heterozygosity. In addition, it was shown that ectopic expression of EI24/P108 resulted in apoptosis, whereas suppression of E124/PIO8 expression resulted in increased survival after treatment with an apoptotic retinoid. We hypothesizid that genetic inactivation of EI24/PIO8 is a major contributing factor to breast cancer development and resistance to chemotherapeutic agents such as etoposide. We recently found evidence that EI24/PIO8 directly binds with Bcl-2 in the endoplasmatic reticulum (ER), and likely initiates apoptosis at this organelle by altering the activity of ER-resident Bcl-2 (purpose of Objectives 1 and 2). Our studies also showed that EI24/PIG8 likely serves to suppress tumor spreading, rather than formation of the primary tumor. Thus, the EI24/PI08 status of breast cancers may serve as a potential novel prognostic indicator in this disease.

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Document Details

Document Type
Technical Report
Publication Date
Mar 01, 2005
Accession Number
ADA433856

Entities

People

  • Remco A. Spanjaard

Organizations

  • Boston University

Tags

DTIC Thesaurus Topics

  • Animal Structures
  • Apoptosis
  • Breast Cancer
  • Carcinoma
  • Cell Physiological Processes
  • Cells
  • Chemistry
  • Chemotherapeutic Agents
  • Chromosomes
  • Cytoplasm
  • Diseases And Disorders
  • Endoplasmic Reticulum
  • Health Services
  • Intracellular Membranes
  • Neoplasms
  • Organelles
  • Resistance

Fields of Study

  • Biology

Readers

  • Breast cancer cell signaling and growth regulation.
  • Cellular and Molecular Pathways of Apoptosis.
  • Molecular and genetic basis of cancer.

Technology Areas

  • Biotechnology