Aspirin-induced Bcl-2 translocation and its phosphorylation in the nucleus trigger apoptosis in breast cancer cells
Experimental & Molecular Medicine
;
: e47-2013.
Article
in English
| WPRIM
| ID: wpr-223715
ABSTRACT
Here, we report that B-cell lymphoma 2 (Bcl-2) is a novel target molecule of aspirin in breast cancer cells. Aspirin influenced the formation of a complex by Bcl-2 and FKBP38 and induced the nuclear translocation of Bcl-2 and its phosphorylation. These events inhibited cancer cell proliferation and subsequently enhanced MCF-7 breast cancer cell apoptosis. Bcl-2 knockdown using small interfering RNA (siRNA) delayed apoptotic cell death, which correlated with increased proliferation following aspirin exposure. In contrast, Bcl-2 overexpression enhanced the onset of aspirin-induced apoptosis, which was also associated with a significant increase in Bcl-2 phosphorylation in the nucleus. Therefore, this study may provide novel insight into the molecular mechanism of aspirin, particularly its anticancer effects in Bcl-2- and estrogen receptor-positive breast cancer cells.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Phosphorylation
/
Protein Binding
/
Cell Nucleus
/
Aspirin
/
Apoptosis
/
Proto-Oncogene Proteins c-bcl-2
/
Tacrolimus Binding Proteins
/
Active Transport, Cell Nucleus
/
MCF-7 Cells
Limits:
Humans
Language:
English
Journal:
Experimental & Molecular Medicine
Year:
2013
Type:
Article
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