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Modeling Spontaneous Metastatic Renal Cell Carcinoma mRCC in Mice Following Nephrectomy
Published on: April 29, 2014
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CA8 promotes RCC proliferation and migration though its expression level is lower in tumor compared to adjacent
Huai-Lu Ma1, Sheng-Jian Yu2, Jie Chen3
1Department of Pharmacology, School of Clinical Medicine, Taizhou University, Taizhou, Zhejiang 318000, China; Graduate School of Medicine, Hebei North University, Zhangjiakou, Hebei 075000, China; School of Medicine, Taizhou University, Taizhou, Zhejiang 318000, China.
Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|November 13, 2019
Summary
Carbonic anhydrase-related protein VIII (CA8) is down-regulated in renal cell carcinoma (RCC) but promotes cancer progression. This study reveals CA8
Area of Science:
- Oncology
- Genetics
- Bioinformatics
Background:
- Renal cell carcinoma (RCC) treatments like chemotherapy and radiotherapy have limited success.
- Targeted therapies offer new avenues, but understanding RCC's genomic landscape is crucial for identifying novel therapeutic targets.
- Integrated genomic analysis can enhance comprehension of RCC and pinpoint new anticancer targets.
Purpose of the Study:
- To investigate the role of Carbonic anhydrase-related protein VIII (CA8) in renal cell carcinoma (RCC) progression.
- To analyze differential mRNA expression and copy number variation (CNV) of CA8 in RCC using bioinformatics.
- To validate CA8's expression and functional impact in RCC cell lines and patient samples.
Main Methods:
- Integrated bioinformatics analysis of The Cancer Genome Atlas (TCGA) database for CA8 expression and CNV.
- RT-PCR and immunohistochemical assays to confirm CA8 mRNA and protein levels in 5 RCC patient samples.
- In vitro assays (MTT, Transwell) to assess the impact of CA8 overexpression and knockdown on RCC cell proliferation and migration.
- In vivo studies using Caki-1 xenografts in mice to evaluate CA8's effect on tumor growth.
- Western blot analysis to examine downstream signaling pathways (pAKT, MMP2).
Main Results:
- CA8 gene exhibited differential mRNA expression and copy number variation (CNV) in RCC.
- CA8 overexpression enhanced the proliferation and migration of Caki-1 and 769-P RCC cells in vitro.
- CA8 overexpression promoted Caki-1 xenograft tumor growth in vivo.
- CA8 knockdown reduced RCC cell proliferation and migration.
- CA8 modulation affected pAKT and MMP2 protein levels, suggesting involvement in signaling pathways.
Conclusions:
- CA8 promotes renal cell carcinoma (RCC) cell proliferation and migration.
- Despite promoting progression, CA8 is found to be down-regulated in RCC.
- Further mechanistic studies are required to understand the contradictory role of CA8 in RCC.
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