2024/07/09 by Haiyang Yan, Zhaohui Xing, Shuai Liu +3 · 1 voice · 1 citation
Biochemistry, Genetics and Molecular Biology · Immunology and Microbiology · #Signaling Pathways in Disease #Immune cells in cancer #Caveolin-1 and cellular processes
paper · pdf · doi:10.18632/aging.205586
openalex publication_date 2024/07/09 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/01
The calcitonin receptor (CALCR) is an essential protein for maintaining calcium homeostasis and has been reported to be upregulated in numerous cancers. However, the molecular role of CALCR in renal cell carcinoma (RCC) is not well understood. In this study, we identified the overexpression of CALCR in RCC using human tissue chip by immunohistochemical (IHC) staining, which was associated with a poor prognosis. Functionally, CALCR depletion inhibited RCC cell proliferation and migration, and induced cell apoptosis and cycle arrest. CALCR is also essential for in vivo tumor formation. Mechanistically, we demonstrated that CALCR could directly bind to CD44, preventing CD44 protein degradation and thereby upregulating CD44 expression. Moreover, a deficiency in CD44 significantly attenuated the promoting role of CALCR on RCC cell proliferation, migration and anti-apoptosis capacities. Collectively, CALCR exacerbates RCC progression via stabilizing CD44, offering a fundamental basis for considering CALCR as a potential therapeutic target for RCC patients.