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Clinical value and mechanism of CDKN2A in clear cell renal cell carcinoma

ABSTRACT: Background: Clear cell renal cell carcinoma (ccRCC) is the most common type of kidney cancer, with its incidence increasing annually. This study aims to investigate the role of the Cyclin-Dependent Kinase Inhibitor 2A (CDKN2A) in ccRCC. Methods: We analyzed ccRCC-related data from the TCGA and GEO databases. First, we systematically assessed the expression levels of CDKN2A and its correlation with clinical features, such as tumor staging and prognosis. Additionally, regarding biological function, we explored the relationship between CDKN2A expression and immune cell infiltration, along with the mechanisms underlying this relationship. We also examined the association between CDKN2A and drug sensitivity through drug sensitivity analysis. Furthermore, we experimentally validated the differential expression of CDKN2A in ccRCC and its impact on the cellular behaviors of ccRCC cells. Results: The results revealed that CDKN2A expression was significantly higher in ccRCC tissues compared to normal kidney tissues, affecting patient prognosis by modulating the tumor microenvironment. Moreover, based on data from the GDSC, and CTRP databases, we found that high CDKN2A expression was closely associated with sensitivity to certain small-molecule drugs. These drugs particularly target the MAPK pathway. Experimental findings indicated that CDKN2A promotes the proliferation, migration, and invasion of ccRCC cells via the MAPK pathway. Conclusions: Our study suggests that CDKN2A has an oncogenic role in ccRCC and may serve as a potential therapeutic target.

ORGANISM(S): Homo sapiens

PROVIDER: GSE309683 | GEO | 2025/10/05

REPOSITORIES: GEO

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	GSE309683_gene_fpkm.txt.gz	Txt

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Project description:The pituitary-tumor transforming gene (PTTG1) is a recently discovered oncogene implicated in the malignant progression of a number of neoplasms. It has been shown to drive both endocrine and non-endocrine malignancies, but has not yet been studied in the context of renal cell carcinoma. Here we show that PTTG1 is frequently amplified and overexpressed in clear cell renal cell carcinoma, the most common form of kidney cancer. Clear cell RCC (ccRCC) is cytogenetically characterized by deletion of chromosome 3p, harboring the von-Hippel Lindau tumor suppressor gene, and amplification of chromosome 5q. The significance of copy number gain of chromosome 5 has to date remained a mystery, but is presumably the location of oncogenes that play an important role in ccRCC development or progression. The PTTG1 oncogene maps to chromosome 5q and shows frequent copy number gain in clear cell RCC, and is significantly overexpressed in tumor tissue relative to adjacent normal kidney. Furthermore, we have established a functional role for PTTG1 in ccRCC tumorigenesis and progression. PTTG1 ablation significantly reduces both the tumorigenic ability of ccRCC cells in vitro and in vivo and the invasive ability of these cells in vitro. An analysis of PTTG1 regulatory targets supports its role in the progression of localized ccRCC to invasive and metastatic disease, an idea further substantiated by PTTG1’s clinical correlation with high grade and high stage tumors and its association with poor prognosis. PTTG1-dependent overexpression of the Rho-GEF ECT2, another proto-oncogene, is observed in a number of ccRCC cell lines, and ECT2 overexpression correlates with PTTG1 overexpression, high stage, high grade, and poor prognosis in human ccRCC tumors. As GEF’s have been promoted as viable drug targets for targeted cancer therapeutics, the relationship between the PTTG1 and ECT2 oncogenes may be able to be exploited for the treatment of this disease. SNP data on 74 ccRCC and 16 normal renal tissue samples were used to profile the cytogenetic gains or losses. The most frequent gains or losses were identified and gene expression data were then used to pinpoint the genes for further study.

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Clinical value and mechanism of CDKN2A in clear cell renal cell carcinoma

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