A20 enhances the radiosensitivity of hepatocellular carcinoma cells to 60Co-γ ionizing radiation
PDF | HTML | Supplementary Files | How to cite
Metrics: PDF 1219 views | HTML 2388 views | ?
Rui Liu1, Dongli Zhao1, Xiaozhi Zhang1, Suxia Han1, Yunyi Yang1, Jinlu Ma1 and Du Meng1
1Department of Radio Oncology, The First Affiliated Hospital of Xi’an Jiaotong University School of Medicine, Xi’an 710061, The People’s Republic of China
Du Meng, email: [email protected]
Keywords: hepatocellular carcinoma, A20, 60Co-γ ionizing radiation, radiotherapy, radiosensitization
Received: June 26, 2017 Accepted: August 07, 2017 Published: October 16, 2017
The radioresistance of hepatocellular carcinoma (HCC) cells is a critical obstacle for effectively applying radiotherapy (RT) in HCC treatment. NF-κB, an important transcription factor, can influence critical cell fate decisions by promoting cell survival or anti-apoptosis in response to cell-stress, e.g. chemotherapies or ionizing radiation (IR). A20, also named as tumor necrosis factor α induced protein 3 (TNFAIP3), is a dominant negative regulator of NF-κB pathway and its functions in HCC are largely unknown. The present work aimed to reveal the role of A20 plays in affecting the radiosensitivity of HCC cells. Higher expression of A20 was detected in hepatic non-tumor cell line or clinical specimens compared with HCC cell lines or clinical specimens. A20 decreased the expression of proteins mediating cellular stress/injury response or epithelial-mesenchymal transition (EMT) process. Overexpression of A20 via adenovirus enhanced the effect of 60Co-γ ionizing radiation (IR) on HCC cells’ injury, e.g. G2/M arrest or DNA double strands break (DSB). Moreover, A20 also enhanced the in vitro or in vivo survival inhibiting of HCC cells induced by IR. These results reveal the roles of A20 in HCC radiosensitization and overexpression of A20 would be a novel strategy for HCC radiotherapy.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.