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PARP-1 promotes autophagy via the AMPK/mTOR pathway in CNE-2 human nasopharyngeal carcinoma cells following ionizing radiation, while inhibition of autophagy contributes to the radiation sensitization of CNE-2 cells

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It was previously reported that poly(adenosine diphosphateribose) polymerase1 (PARP1) regulated ionizing radiation (IR)induced autophagy in CNE2 human nasopharyngeal carcinoma cells. The present study aimed to investigate whether PARP1mediated IRinduced autophagy occurred via activation of the liver kinase B1 (LKB1)/adenosine monophosphateactivated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signaling pathway in CNE2 cells. In addition, the effect of PARP1 and AMPK inhibition on the radiation sensitization of CNE2 cells was investigated. CNE2 cells were treated with 10 Gy IR in the presence or absence of the AMPK activator 5amino1βDribofuranosyl1Himidazole4carboxamide (AICAR). In addition, IRtreated CNE2 cells were transfected with lentivirusdelivered smallhairpin RNA or treated with the AMPK inhibitor Compound C. Western blot analysis was used to assess the protein expression of PARP1, phosphorylated (p)AMPK, microtubuleassociated protein 1 light chain 3 (LC3) and pP70S6K. Cell viability and clone formation assays were performed to determine the effect of PARP1 silencing and AMPK inhibition on the radiation sensitization of CNE2 cells. The results showed that IR promoted PARP1, pAMPK and LC3 protein expression as well as decreased pP70S6K expression compared with that of the untreated cells. In addition, AICAR increased the expression of pAMPK and LC3 as well as decreased pP70S6K expression compared with that of the IRonly group; however, AICAR did not increase PARP1 expression. Furthermore, PARP1 gene silencing decreased the expression of PARP1, pAMPK and LC3 as well as increased pP70S6K expression. Compound C decreased pAMPK and LC3 expression as well as increased pP70S6K expression; however, Compound C did not increase PARP1 expression. Western blot analysis detected limited expression of pLKB1 in all treatment groups. Cell viability and clone formation assays revealed that PARP1 or AMPK inhibition reduced the proliferation of CNE2 cells following IR. In conclusion, the present study demonstrated that PARP1 promoted autophagy via the AMPK/mTOR pathway; in addition, PARP1 or AMPK inhibition contributed to the radiation sensitization of CNE2 cells following IR. However, it remains to be elucidated whether PARP1 is an upstream mediator of the LKB1 pathway in CNE2 cells following IR.
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Document Type: Research Article

Affiliations: Department of Radiation Oncology, Affiliated Cancer Hospital of Guangxi Medical University, Cancer Institute of Guangxi Zhuang Autonomous Region, Nanning, Guangxi 530021, P.R. China

Publication date: August 1, 2015

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  • Molecular Medicine Reports is a monthly, peer-reviewed journal available in print and online, that includes studies devoted to molecular medicine, underscoring aspects including pharmacology, pathology, genetics, neurosciences, infectious diseases, molecular cardiology and molecular surgery. In vitro and in vivo studies of experimental model systems pertaining to the mechanisms of a variety of diseases offer researchers the necessary tools and knowledge with which to aid the diagnosis and treatment of human diseases.
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