Potential involvement of cuproptosis induced by m6A-modified autophagy gene ATG10 in KICH

Kidney Chromophobe (KICH) is the third most prevalent renal malignancy, with research challenges due to a dearth of cell lines and clinical samples. There is no specific treatment regimen tailored exclusively for KICH. This study employed gene expression analysis, immunohistochemistry (IHC), Spearman's correlation, immune cell infiltration assessment, and molecular network construction to investigate the autophagy gene ATG10 in KICH. ATG10 was uniquely downregulated in KICH, predominantly regulated by RNA m6A methylation. This downregulation correlated with patient survival, suggesting a potential tumor-regulatory role. ATG10's involvement in the protein lipidation pathway, essential for cuproptosis, was identified. B cells and CD8 + T cells were key immune cells in KICH tumorigenesis associated with ATG10. Examination of molecular networks identified several key molecules and mechanisms, including ceRNA, interplaying proteins, and transcription factors. Additionally, drug targeting analysis pointed to specific amino acids and metabolites as potential therapeutic agents. This study elucidates the significance of ATG10 in KICH, implicating m6A methylation and cuproptosis as novel targets for therapeutic intervention. The identification of B cells and CD8 + T cells as key immune components, along with specific amino acids, suggests that a combination of targeted immune therapies and dietary interventions could provide a multifaceted approach to KICH treatment. Given the limited understanding of KICH pathogenesis, our analysis has unveiled new theoretical insights and potential clinical significances for KICH, expected to broaden the research horizon in this field.