Journal
GENE
Volume 832, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.gene.2022.146559
Keywords
SELS; ccRCC; GSK3 beta; NF-kappa B; Proliferation; Apoptosis
Categories
Funding
- 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]
Ask authors/readers for more resources
SELS is highly expressed in clear cell renal cell carcinoma (ccRCC) and associated with multiple pathological features. SELS overexpression promotes cell proliferation and inhibits apoptosis, while silence of SELS has the opposite effect. Mechanistically, SELS activates AKT/GSK3 beta/NF-kappa B signaling pathway to enhance cell proliferation and inhibit apoptosis, and stabilizes c-Myc by preventing ubiquitin-proteasome-mediated degradation. Furthermore, SELS inhibits ccRCC cell migration likely through repressing epithelial-mesenchymal transition (EMT).
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available