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Purpose <p>Clear cell renal cell carcinoma (ccRCC) is resistant to radiotherapy and chemotherapy. Thus, it is necessary to find new diagnostic markers and therapeutic targets to increase the overall outcomes of ccRCC. Recent studies have shown that therapeutic methods that interfere with the energy transfer system can also positively affect the treatment process.</p> Methods <p>The present study is focused on finding markers associated with mitochondrial metabolic pathways that affect the outcome of ccRCC. For this purpose, we investigated various aspects of the relationship between mitochondrial metabolism and ccRCC based on analysis of gene network connections and differentially expressed genes, through assessment of protein–protein interaction, mutations, and promoter methylation on the related genes. We also investigated gene interaction with miRNAs and immune infiltration analysis.</p> Results <p>Through these steps, we provided a list of possible diagnostic markers and therapeutic targets for ccRCC.</p> Conclusion <p>The current study further proved the importance of mitochondrial metabolic pathways in the pathogenesis of ccRCC and provided a list of possible diagnostic markers and therapeutic targets from these pathways that can be used in ccRCC.</p>

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Bioinformatics analysis of mitochondrial metabolism-related genes demonstrates their importance in renal cell carcinoma

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年1月9日

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  • Mohsen Ahmadi,
  • Maryam Motallebinezhad,
  • Pegah Mousavi,
  • Amir Hossein Miladipour,
  • Shamim Fooladgar,
  • Soudeh Ghafouri-Fard,
  • Seyed Amirhossein Fazeli

摘要

Purpose

Clear cell renal cell carcinoma (ccRCC) is resistant to radiotherapy and chemotherapy. Thus, it is necessary to find new diagnostic markers and therapeutic targets to increase the overall outcomes of ccRCC. Recent studies have shown that therapeutic methods that interfere with the energy transfer system can also positively affect the treatment process.

Methods

The present study is focused on finding markers associated with mitochondrial metabolic pathways that affect the outcome of ccRCC. For this purpose, we investigated various aspects of the relationship between mitochondrial metabolism and ccRCC based on analysis of gene network connections and differentially expressed genes, through assessment of protein–protein interaction, mutations, and promoter methylation on the related genes. We also investigated gene interaction with miRNAs and immune infiltration analysis.

Results

Through these steps, we provided a list of possible diagnostic markers and therapeutic targets for ccRCC.

Conclusion

The current study further proved the importance of mitochondrial metabolic pathways in the pathogenesis of ccRCC and provided a list of possible diagnostic markers and therapeutic targets from these pathways that can be used in ccRCC.