Related Experiment Video
Updated: Jun 21, 2025
05:36
Comparing Metastatic Clear Cell Renal Cell Carcinoma Model Established in Mouse Kidney and on Chicken Chorioallantoic Membrane
Published on: February 8, 2020
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CALCR exacerbates renal cell carcinoma progression via stabilizing CD44
Haiyang Yan1, Zhaohui Xing2, Shuai Liu3
1Department of Urology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, China.
Aging
|July 10, 2024
Summary
Calcitonin receptor (CALCR) overexpression promotes renal cell carcinoma (RCC) progression by stabilizing CD44, indicating CALCR as a potential therapeutic target for kidney cancer.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Calcitonin receptor (CALCR) is crucial for calcium homeostasis and implicated in various cancers.
- The specific role of CALCR in renal cell carcinoma (RCC) remains largely unelucidated.
Purpose of the Study:
- To investigate the role and mechanism of CALCR in RCC progression.
- To evaluate CALCR as a potential therapeutic target for RCC.
Main Methods:
- Immunohistochemical (IHC) staining on human tissue chips to assess CALCR expression in RCC.
- Functional assays involving CALCR depletion in RCC cell lines (proliferation, migration, apoptosis, cell cycle).
- In vivo tumor formation studies and mechanistic investigations of CALCR-CD44 interaction.
Main Results:
- CALCR was found to be overexpressed in RCC, correlating with poor prognosis.
- CALCR depletion inhibited RCC cell proliferation, migration, induced apoptosis, and cell cycle arrest.
- CALCR directly binds to CD44, preventing its degradation and increasing its expression, which is crucial for CALCR's pro-tumorigenic effects.
Conclusions:
- CALCR exacerbates RCC progression by stabilizing CD44.
- CALCR represents a promising therapeutic target for renal cell carcinoma patients.
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