Down-Regulation of PER2 Increases Apoptosis of Gliomas after X-Ray IrradiationLei Yin1, Wenbin Liu2, Hechun Xia1,2* Xiaoxiong Jia1,2 and David Leavesley3
- *Corresponding Author:
- Hechun Xia
Department of Neurosurgery, General Hospital of Ningxia Medical University
Shengli Street, Yinchuan, 750004, Ningxia, PR China
Tel: + 8613995109559
E-mail: [email protected]
Received date: December 28, 2016; Accepted date: March 28, 2017; Published date: April 04, 2017
Citation: Yin L, Liu W, Xia H, Jia X, Leavesley D (2017) Down-Regulation of PER2 Increases Apoptosis of Gliomas after X-Ray Irradiation. Chemo Open Access 6:228. doi: 10.4172/2167-7700.1000228
Copyright: © 2017 Yin L, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Period2 (PER2), a core circadian gene, not only modulates circadian rhythm but also may play an important role in other biological processes including pathways involved in the proliferation and apoptosis of tumor cells. In this study, we investigated the mechanism by which downregulated expression of PER2 promotes apoptosis of wild-type TP53 human glioma U343 cells exposed to X-rays. U343 cells were irradiated with 6mV 10Gy X-ray irradiation after infection with shRNA lentivirus to reduce expression of PER2, and then analyzed by several methods such as SCGE analysis, flow cytometry, RT-PCR, and western blotting. Compared with controls, U343 cells expressing low levels of PER2 showed serious DNA damage when exposed to X-ray irradiation in SCGE analysis (P<0.05), and higher death rates in flow cytometry assay (P<0.05). RT-PCR and western blot analysis both revealed decreased expression of ATM and TP53, which regulate DNA damage and repair via the ATM-TP53 pathway, and an increased expression of C-MYC, which is related to cell apoptosis. Thus, our research suggests that PER2 may play an important role in tumor radiotherapy, which is attributable to enhanced ATM-TP53 signaling and pro-apoptotic processes. These findings provide a new target for the clinical treatment of glioma, and a reliable basis for postradiation therapy and gene therapy for glioma and other cancers.