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SOCS1 counter-acts the ROS-mediated survival signals and promotes apoptosis with cell cycle modulation to increase radiosensitivity of colorectal cancer cells
Ji-Yoon Ryu1 (Graduate Student), Jiyoung Oh1 (Graduate Student), Su-Min Kim1 (Graduate student), Won-Gi Kim1,2 (Graduate student), Hana Jeong1 (Graduate student), Seol-Hee Kim1 (Graduate student), Sinae Ahn1 (Graduate student), Byong Chul Yoo2 (Research Associate), Choong-Eun Lee 1,* (Professor)
1Department of Biological Science, Sungkyunkwan University, Korea,
2Colorectal Cancer Branch, Research Center, National CAncer Institute, Korea
As negative regulators of cytokine signaling pathways, suppressors of cytokine signaling (SOCS) proteins have been reported for both pro-tumor and anti-tumor functions. Since our recent studies have demonstrated suppressive effects of SOCS1 on epithelial to mesenchymal signaling in colorectal cancer cells in response to fractionated ionizing radiation or oxidative stress, we have studied radiosensitizing action of SOCS1 as an anti-tumor mechanism in this tumor cell model. In HCT116 cells exposed to ionizing radiation, SOCS1 over-expression shifted cell cycle arrest from G2/M to G1 and led to the promotion of radiation-induced apoptosis in p53-dependent manners, with down-regulation of cyclin B and up-regulation of p21. On the other hand, SOCS1 knock-down resulted in a reduced apoptosis with the decrease in G1 arrest. The regulatory action of SOCS1 on the radiation response was mediated by inhibition of radiation-induced Jak3/STAT3 and Erk activities thereby blocking G1 to S transition. The radiation-induced early ROS signal was responsible for the activation of Jak3/ Erk/STAT3 leading to cell survival response, which was inhibited by SOCS1 and promoted by shSOCS1. The data collectively indicate that SOCS1 promotes radiosensitivity of colorectal cancer cells by counter-acting ROS-mediated survival signal thereby blocking cell cycle progression from G1 to S. The resulting increase in G1 arrest with p53 activation then contributes to the promotion of apoptotic response upon radiation. The induction of SOCS1 expression thus may increase therapeutic efficacy of radiation in tumors with low SOCS1 levels.
Abstract, Accepted Manuscript(in press) [Submitted on December 31, 2021, Accepted on March 3, 2022]
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