Gαi3 nuclear translocation causes irradiation resistance in human glioma cells
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Shang Cai1,*, Ya Li2,*, Jin-Yu Bai3,*, Zhi-Qing Zhang2,*, Yin Wang2, Yin-Biao Qiao4, Xiao-Zhong Zhou3, Bo Yang4, Ye Tian1, Cong Cao2
1Department of Radiotherapy and Oncology, The Second Affiliated Hospital of Soochow University, Suzhou, China
2Institute of Neuroscience, Soochow University, Suzhou, China
3Department of Orthopedics, The Second Affiliated Hospital of Soochow University, Suzhou, China
4Department of Surgery, The Third Hospital affiliated to Soochow University, Suzhou, China
Bo Yang, email: email@example.com
Cong Cao, email: firstname.lastname@example.org
Keywords: glioma, irradiation, Gαi3, DNA-PKcs
Received: March 13, 2017 Accepted: March 30, 2017 Published: April 11, 2017
We have previously shown that Gαi3 is elevated in human glioma, mediating Akt activation and cancer cell proliferation. Here, we imply that Gαi3 could also be important for irradiation resistance. In A172 human glioma cells, Gαi3 knockdown (by targeted shRNAs) or dominant-negative mutation significantly potentiated irradiation-induced cell apoptosis. Reversely, forced over-expression of wild-type or constitutively-active Gαi3 inhibited irradiation-induced A172 cell apoptosis. Irradiation in A172 cells induced Gαi3 translocation to cell nuclei and association with local protein DNA-dependent protein kinase (DNA-PK) catalytic subunit. This association was important for DNA damage repair. Gαi3 knockdown, depletion (using Gαi3 knockout MEFs) or dominant-negative mutation potentiated irradiation-induced DNA damages. On the other hand, expression of the constitutively-active Gαi3 in A172 cells inhibited DNA damage by irradiation. Together, these results indicate a novel function of Gαi3 in irradiation-resistance in human glioma cells.
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