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CD24 enhances DNA damage-induced apoptosis by modulating NF-kappa B signaling in CD44-expressing breast cancer cells

Title
CD24 enhances DNA damage-induced apoptosis by modulating NF-kappa B signaling in CD44-expressing breast cancer cells
Author
신인철
Keywords
apoptosis; doxorubicin; signal transduction; cell proliferation; cd44 antigens; dna; phosphotransferases; transfection; homing-associated cell adhesion molecule; breast cancer cell; attenuation; molecule; mcf-7 cells
Issue Date
2011-10
Publisher
OXFORD UNIV PRESS, GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
Citation
CARCINOGENESIS, 32, 10, 1474-1483
Abstract
Cluster of differentiation 24 (CD24) is a small glycosylphosphatidylinositol-linked cell surface molecule that is expressed in a variety of human carcinomas, including breast cancer. To determine the role of CD24 in breast cancer cells, we expressed CD24 in CD24-negative/low and cluster of differentiation 44 (CD44)-positive MDA-MB-231 metastatic breast cancer cells. Forced expression of CD24 resulted in a decrease in c-Raf/mitogen-activated protein/extracellular signal-regulated kinase kinase (MEK)/mitogen-activated protein kinase signaling and reduced cell proliferation. Apoptosis induced by DNA damage was greatly enhanced in MDA-MB-231 CD24 cells as compared with MDA-MB-231 vec cells. CD24 expression efficiently attenuated DNA damage-induced nuclear factor-kappaB (NF-kappa B) signaling in MDA-MB-231 cells. However, in CD24-positive and CD44-negative/low MCF-7 cells, knockdown of CD24 did not significantly affect DNA damage-induced apoptosis nor NF-kappa B signaling. Silencing of CD24 in CD24/CD44-double-positive MDA-MB-468 cells partially rescued DNA damage-induced apoptosis. Transient transfection studies with 293T cells also revealed that CD24 attenuated cell viability and NF-kappa B signaling only when CD44 was cotransfected. These data indicate that CD24 expression potentiated DNA-induced apoptosis by suppressing antiapoptotic NF-kappa B signaling in CD44-expressing cells.
URI
https://academic.oup.com/carcin/article/32/10/1474/2463725
ISSN
0143-3334
DOI
10.1093/carcin/bgr173
Appears in Collections:
COLLEGE OF NATURAL SCIENCES[S](자연과학대학) > LIFE SCIENCE(생명과학과) > Articles
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