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PMID: 19379710 Published · ppublish English Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Review

Molecular mechanisms controlling E-cadherin expression in breast cancer.

Biochemical and biophysical research communications ·Vol. 384 ·No. 1 ·2009-06-19 ·Pages 6-11

Baranwal S, Alahari SK

Abstract

Disruption of cell-cell adhesion, which is essential for the maintenance of epithelial plasticity and is mediated by a class of proteins called cadherins, is an initial event in the progression of cancer. Cadherins are Ca(2+)-dependent transmembrane proteins that are associated with actin via other cytoplasmic proteins. Disruption of cell-cell adhesion during cancer progression is an important event during cancer initiation and metastasis. E-cadherin, one of the most widely studied tumor suppressors in breast cancer, belongs to a family of calcium-dependent cell adhesion molecules. Various signaling molecules and transcription factors regulate the expression of E-cadherin. Loss of E-cadherin has been reported to induce epithelial-mesenchymal transition in several cancers. This review highlights recent advances in defining the mechanisms that regulate E-cadherin expression in breast cancer.

MeSH Terms
Breast Neoplasms/genetics,pathology Cadherins/genetics Cell Adhesion/genetics Gene Expression Regulation, Neoplastic Humans Transcription, Genetic
Chemicals
Cadherins
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Baranwal Somesh
Department of Biochemistry and Molecular Biology, LSU Health Science Center, New Orleans, LA 70112, USA.
Alahari Suresh K
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Article Info
Journal
Biochemical and biophysical research communications
Abbr.
Biochem Biophys Res Commun
ISSN
1090-2104
DOI
10.1016/j.bbrc.2009.04.051
Published
2009-06-19
Epub
2009-00-18
Pages
6-11
Language
English
Region
United States
NLM ID
0372516
PMCID
PMC2700729
Subset
IM
Grants
NCI NIH HHS · R01 CA115706 · United States
NCI NIH HHS · R01 CA115706-02 · United States
NCI NIH HHS · CA115706 · United States
External Links
PubMed source DOI: 10.1016/j.bbrc.2009.04.051 PMC Full Text View journal details
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