Aging
Navigate
Submit an Article
Research Paper|Volume 16, Issue 13|pp 10765—10783

CALCR exacerbates renal cell carcinoma progression via stabilizing CD44

Haiyang Yan1, Zhaohui Xing2, Shuai Liu3, Peng Gao1, Qingli Wang1, Guiying Guo1
  • 1Department of Urology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, China
  • 2Department of Urology, Heilongjiang Provincial Hospital, Harbin, Heilongjiang 150036, China
  • 3Department of Urology, The Third Affiliated Hospital of Qiqihar Medical College, Qiqihaer, Heilongjiang 161099, China
Received: June 13, 2023Accepted: January 4, 2024Published: July 9, 2024
https://doi.org/10.18632/aging.205586

Copyright: © 2024 Yan et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

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.