期刊
GENE
卷 832, 期 -, 页码 -出版社
ELSEVIER
DOI: 10.1016/j.gene.2022.146559
关键词
SELS; ccRCC; GSK3?; NF-K=kB; Proliferation; Apoptosis
资金
- National Natural Science Foundation of China [82030065, 81873932, 81973567]
- Xian Municipal Health Commission Fund [2020yb04]
- Chongqing Science and Technology Commission Fund Project [cstc2021jcyj-msxmX0312]
- Xian Science and Technology Commission Fund Project [21YXYJ0032]
SELS is significantly upregulated in ccRCC and promotes tumor progression, inhibits apoptosis, and migration by activating the AKT/GSK3 beta/NF-kappa B signaling pathway and repressing EMT.
Clear cell renal cell carcinoma (ccRCC) is one of the most lethal genitourinary tumors with rapid progression and metastasis. Selenoprotein 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 clinicopathological features. Overexpression of SELS could promote cell proliferation and inhibit apoptosis in 786-O 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.
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