Selenoprotein S regulates tumorigenesis of clear cell renal cell carcinoma through AKT/ GSK3 beta/NF-kappa B signaling pathway

作者全名："Mao, Huajie; Zhao, Ya; Lei, Li; Hu, Yanxia; Zhu, Hangrui; Wang, Runzhi; Ni, Dongsheng; Liu, Jianing; Xu, Lei; Xia, Hua; Zhang, Zaikuan; Ma, Meng; Pan, Zheng; Zhou, Qin; Xie, Yajun"

作者地址："[Mao, Huajie; Zhao, Ya; Lei, Li; Hu, Yanxia; Zhu, Hangrui; Wang, Runzhi; Ni, Dongsheng; Liu, Jianing; Xu, Lei; Xia, Hua; Zhang, Zaikuan; Ma, Meng; Zhou, Qin; Xie, Yajun] Chongqing Med Univ, Coll Lab Med, Key Lab Lab Med Diagnost, Minist Educ, Chongqing 400016, Peoples R China; [Mao, Huajie; Zhao, Ya] First Hosp Xian, Dept Lab Med, Xian 710002, Peoples R China; [Pan, Zheng] Chongqing Med Univ, Coll Tradit Chinese Med, Chongqing 400016, Peoples R China"

通信作者："Xie, YJ (通讯作者)，Chongqing Med Univ, Coll Lab Med, 1 Yixueyuan Rd, Chongqing 400016, Peoples R China."

来源：GENE

ESI学科分类：MOLECULAR BIOLOGY & GENETICS

WOS号：WOS:000877491100004

JCR分区：Q2

影响因子：3.5

年份：2022

卷号：832

期号：　

开始页：　

结束页：　

文献类型：Article

关键词：SELS; ccRCC; GSK3 beta; NF-kappa B; Proliferation; Apoptosis

摘要："Clear cell renal cell carcinoma (ccRCC) is one of the most lethal genitourinary tumors with rapid progression and metastasis. Selenopmtein S (SELS), which is broadly expressed in human tissues, has been reported to be involved in ER homeostasis and inflammation. However, the biological roles of SELS in ccRCC remain unclear. In this study, we found that SELS expression was significantly higher in ccRCC and correlated with multiple dinicopathological features. Overexpression of SELS could promote cell proliferation and inhibit apoptosis in 786-0 cells, whereas silence of SELS elicited opposite effect. Further mechanistic studies revealed that SELS enhanced cell proliferation and inhibited apoptosis through activating AKT/GSK3 beta/NF-kappa B signaling pathway. Besides, SELS could stabilize c-Myc by preventing ubiquitin-proteasome-mediated degradation. Interestingly, we found that SELS could also inhibit migration of ccRCC cell likely through repressing epithelial-mesenchymal transition (EMT). Collectively, our findings suggested that SELS promoted tumor progression, and inhibited apoptosis and migration through AKT/GSK3 beta/NF-kappa B signaling pathway and EMT in ccRCC."

基金机构："National Natural Science Foundation of China [82030065, 81873932, 81973567]; Municipal Health Commission Fund Project [2020yb04]; Chongqing Science and Technology Commission Fund Project [cstc2021jcyj-msxmX0312]; Xi'an Science and Science and Technology Commission Fund Project [21YXYJ0032]"

基金资助正文："This research was funded by National Natural Science Foundation of China (Grant No. 82030065, 81873932 and 81973567), Xi'an Municipal Health Commission Fund Project (grants number 2020yb04), Chongqing Science and Technology Commission Fund Project (grants number cstc2021jcyj-msxmX0312) and Xi'an Science and Technology Commission Fund Project(grants number 21YXYJ0032).The authors are thankful for all the fellows in the M.O.E. Key Laboratory of Laboratory Medical Diagnostics, the College of Laboratory Medicine, Chongqing Medical University."