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Key sunitinib-related biomarkers for renal cell carcinoma
Yun Peng1, Shiqiang Dong1, Yuxuan Song2
1Tianjin Institute of Urology, The 2nd Hospital of Tianjin Medical University, Tianjin, China.
Background:
Renal cell carcinoma (RCC) contributed to 403,262 new cases worldwide in 2018, which constitutes 2.2% of global cancer, nevertheless, sunitinib, one of the major targeted therapeutic agent for RCC, often developed invalid due to resistance. Emerging evidences suggested sunitinib can impact tumor environment which has been proven to be a vital factor for tumor progression.
Methods:
In the present study, we used ssGSEA to extract the immune infiltrating abundance of clear cell RCC (ccRCC) and normal control samples from GSE65615, TCGA, and GTEx; key immune cells were determined by Student's t-test and univariable Cox analysis. Co-expression network combined with differentially expressed analysis was then applied to derive key immune-related genes for ccRCC, followed by the identification of hub genes using differential expression analysis. Subsequently, explorations and validations of the biological function and the immune-related and sunitinib-related characteristics were conducted in KEGG, TISIDB, Oncomine, ICGC, and GEO databases.
Results:
We refined immature dendritic cells and central memory CD4 T cells which showed associations with sunitinib and ccRCC. Following, five hub genes (CRYBB1, RIMBP3C, CEACAM4, HAMP, and LYL1) were identified for their strong relationships with sunitinib and immune infiltration in ccRCC. Further validations in external data refined CRYBB1, CEACAM4, and HAMP which play a vital role in sunitinib resistance, immune infiltrations in ccRCC, and the development and progression of ccRCC. In conclusion, our findings could shed light on the resistance of sunitinib in ccRCC and provide novel biomarkers or drug targets for ccRCC.
Insights
Sunitinib resistance in renal cell carcinoma (RCC) was investigated. Researchers identified key genes (CRYBB1, CEACAM4, HAMP) linked to sunitinib resistance and immune infiltration in clear cell RCC (ccRCC), offering potential new therapeutic targets.
Area of Science:
- Oncology
- Immunology
- Genetics
Background:
- Renal cell carcinoma (RCC) is a significant global cancer burden.
- Sunitinib is a key targeted therapy for RCC but faces challenges due to drug resistance.
- Tumor microenvironment modulation by sunitinib is crucial for cancer progression.
Purpose of the Study:
- To investigate the mechanisms of sunitinib resistance in clear cell renal cell carcinoma (ccRCC).
- To identify key immune cells and genes associated with sunitinib response and ccRCC progression.
- To discover novel biomarkers and therapeutic targets for ccRCC.
Main Methods:
- Utilized ssGSEA to analyze immune cell infiltration in ccRCC and normal samples from multiple datasets (GSE65615, TCGA, GTEx).
- Employed Student's t-test and univariable Cox analysis to identify key immune cells.
- Applied co-expression network and differential expression analyses to identify hub genes related to ccRCC and sunitinib resistance.
- Validated findings using KEGG, TISIDB, Oncomine, ICGC, and GEO databases.
Main Results:
- Immature dendritic cells and central memory CD4 T cells were associated with sunitinib and ccRCC.
- Five hub genes (CRYBB1, RIMBP3C, CEACAM4, HAMP, LYL1) showed strong links to sunitinib, immune infiltration, and ccRCC.
- CRYBB1, CEACAM4, and HAMP were further validated as crucial for sunitinib resistance, immune infiltration, and ccRCC development.
Conclusions:
- Identified specific genes (CRYBB1, CEACAM4, HAMP) as vital players in sunitinib resistance and ccRCC progression.
- These findings offer insights into overcoming sunitinib resistance in ccRCC.
- The identified genes represent potential novel biomarkers or drug targets for ccRCC treatment.
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