Journal
NUTRITION RESEARCH
Volume 47, Issue -, Pages 63-71Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.nutres.2017.09.001
Keywords
Punicalagin; Papillary thyroid carcinoma; BCPAP cell; DNA damage response; Ataxia-telangiectasia mutated gene-encoded protein
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Funding
- National Natural Science Foundation of China [81402214, 81602352, 81422050]
- Research Innovation Program of academic degree postgraduates in colleges and universities in Jiangsu Province [KYZZ16_0061]
- Wuxi Health and Family Planning Commission Foundation [Q201608]
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Punicalagin (PUN), a component derived from pomegranate, is well known for its anticancer activity. Our previous work revealed that PUN induces autophagic cell death in papillary thyroid carcinoma cells. We hypothesized that PUN triggers DNA damage associated with cell death because DNA damage was reported as an inducer of autophagy. Our results showed that PUN treatment caused DNA breaks as evidenced by the significant enhancement in the phosphorylation of H2A.X. However, reactive oxygen species and DNA conformational alteration, 2 common inducing factors in DNA damage, were not involved in PUN-induced DNA damage. The phosphorylation of ataxia-telangiectasia mutated gene-encoded protein (ATM) but not ataxia telangiectasia and Rad3-related protein (ATR) was up-regulated in a time- and dosage-dependent manner after PUN treatment. KU-55933, an inhibitor of ATM, inhibited the phosphorylation of ATM induced by PUN and reversed the decreased cell viability caused by PUN. Thus, we demonstrated that PUN induces cell death of papillary thyroid carcinoma cells by triggering ATM-mediated DNA damage response, which provided novel mechanisms and potential targets for the better understanding of the anticancer actions of PUN. (C) 2017 Elsevier Inc. All rights reserved.
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