Bisdemethoxycurcumin enhances X-ray-induced apoptosis possibly through p53/Bcl-2 pathway.

Citation data:

Mutation research, ISSN: 1873-135X, Vol: 815, Page: 1-5

Publication Year:
2017
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PMID:
28283087
DOI:
10.1016/j.mrgentox.2016.12.005
Author(s):
Enomoto, Atsushi, Yamada, Junko, Morita, Akinori, Miyagawa, Kiyoshi
Publisher(s):
Elsevier BV
Tags:
Biochemistry, Genetics and Molecular Biology, Environmental Science
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article description
Bisdemethoxycurcumin (BDMC), which is isolated from the rhizomes of Curcuma longa, has anti-inflammatory and anti-carcinogenic activities. Here we found that BDMC enhanced X-ray-induced apoptosis in human T-cell leukemia MOLT-4 cells. Knockdown of p53 significantly attenuated the radiosensitizing effect of BDMC. However, BDMC did not enhance X-ray-mediated activation of the p53 signaling pathway via p53's transactivation or mitochondrial translocation. On the other hand, BDMC promoted the X-ray-induced dephosphorylation at Ser 70 in Bcl-2's flexible loop regulatory domain and Bcl-2 binding to p53. Overexpressing Bcl-2 completely blocked the BDMC's radiosensitization effect. Our results indicate that BDMC stimulates the dephosphorylation and p53-binding activity of Bcl-2 and suggest that BDMC may induce a neutralization of Bcl-2's anti-apoptotic function, thereby enhancing X-ray-induced apoptosis.

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