Bit1 in anoikis resistance and tumor metastasis.

TitleBit1 in anoikis resistance and tumor metastasis.
Publication TypeJournal Article
Year of Publication2013
AuthorsJenning S, Pham T, Ireland SKale, Ruoslahti E, Biliran H
JournalCancer Lett
Volume333
Issue2
Pagination147-51
Date Published2013 Jun 10
ISSN1872-7980
KeywordsAnimals, Anoikis, Apoptosis, Carboxylic Ester Hydrolases, Epithelial Cells, Extracellular Matrix, Humans, Mitochondrial Proteins, Neoplasm Metastasis
Abstract

Epithelial cells and most adherent normal cells rely on adhesion-dependent, integrin-mediated survival signals from the extracellular matrix (ECM) to survive. When these cells are deprived of adhesion to the ECM, they undergo a specific form of apoptosis termed "anoikis." In contrast, malignant cells have attained mechanisms to enable them to survive in the absence of adhesion and are considered anchorage-independent. This review will focus on the biological function of the Bcl2-inhibitor of transcription (Bit1) protein in the anoikis process, the underlying molecular mechanism of Bit1 apoptotic function, and its role in tumor metastasis.

DOI10.1016/j.canlet.2013.01.043
Alternate JournalCancer Lett.
PubMed ID23376255
PubMed Central IDPMC3651913
Grant List1R15CA158677-01A1 / CA / NCI NIH HHS / United States
CA30199 / CA / NCI NIH HHS / United States
G12 MD007595 / MD / NIMHD NIH HHS / United States
G12 RR026260 / RR / NCRR NIH HHS / United States
R15 CA158677 / CA / NCI NIH HHS / United States
RCMI G12RR026250-03 / RR / NCRR NIH HHS / United States
SC2 CA153382 / CA / NCI NIH HHS / United States
SC2CA153382 / CA / NCI NIH HHS / United States