Exp Mol Med.  2013 Oct;45(10):e47.

Aspirin-induced Bcl-2 translocation and its phosphorylation in the nucleus trigger apoptosis in breast cancer cells

• Choi BH
• Chakraborty G
• Baek K
• Yoon HS

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.

Keyword

apoptosis; aspirin; Bcl-2; breast cancer; FKBP38; MCF-7

MeSH Terms

Active Transport, Cell Nucleus/drug effects
*Apoptosis
Aspirin/*pharmacology
Cell Nucleus/*metabolism
Humans
MCF-7 Cells
Phosphorylation
Protein Binding
Proto-Oncogene Proteins c-bcl-2/genetics/*metabolism
Tacrolimus Binding Proteins/metabolism
Aspirin
Proto-Oncogene Proteins c-bcl-2
Tacrolimus Binding Proteins