Novel approaches for chemosensitization of breast cancer cells: The E1A story

Yong Liao, Dihua Yu, Mien Chie Hung

Research output: Chapter in Book/Report/Conference proceedingChapter

17 Scopus citations

Abstract

The adenoviral E1A-mediated sensitization to a variety of anti-cancer drug-induced apoptosis is a well-established phenomenon on different types of cell systems. However, the mechanisms underlying E1A-mediated chemosensitization are still not fully understood. Recent studies demonstrate that E1A-mediated sensitization to drug-induced apoptosis can occur via multiple pathways; some of which depend on the expression of functional p53 and/or p19ARF proteins, while some are not. In human breast cancer cells with Her-2/neu overexpression, which usually are more resistance to anti-cancer drugs than cells without Her-2/neu overexpression, may be sensitized through E1A-mediated downregulation of Her-2/neu. Alternatively, E1A can induce sensitization to anticancer drugs in cancer cells or normal diploid fibroblast cells through upregulating the expression of caspase proenzymes, or downregulating the activity of a critical survival factor Akt and/or upregulating the activities of a pro-apoptotic kinase p38 and a protein phosphatase PP2A, etc. This review summarizes these progresses and proposes a plausible feed-forward model for E1A-mediated chemosensitization in human breast cancer cells.

Original languageEnglish (US)
Title of host publicationBreast Cancer Chemosensitivity
EditorsDihua Yu, Mien-Chie Hung
Pages144-169
Number of pages26
DOIs
StatePublished - 2007

Publication series

NameAdvances in Experimental Medicine and Biology
Volume608
ISSN (Print)0065-2598

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology

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