Identification of CHMP7 as a promising immunobiomarker for immunotherapy and chemotherapy and impact on prognosis of colorectal cancer patients

Introduction: ESCRT is a molecular machine involved in various important physiological processes, such as the formation of multivesicular bodies, cellular autophagy, and cellular membrane repair. CHMP7 is a regulatory subunit of ESCRT-III and is necessary for the proper functioning of ESCRT. In this study, public databases were exploited to explore the role of CHMP7 in tumors. Methods: The research on CHMP7 in oncology is rather limited. In this study, the differential expression of CHMP7 in multiple tumor tissues was analyzed with information from public databases and clinically collected colorectal cancer tissue samples. Subsequently, the mutational landscape of CHMP7, methylation levels, and the relationship between its expression levels and genomic instability were resolved. The immune microenvironment is a compelling emerging star in tumor research. The correlation of CHMP7 with various infiltrating immune cell types in TME was analyzed by online datasets and single-cell sequencing. In terms of clinical treatment, the impact of CHMP7 expression levels on chemotherapy and immunotherapy and the evaluation of small molecule drugs related to CHMP7 were assessed. Results: CHMP7 has a predictive value for the prognosis of patients with tumors and is highly involved in tumor immunity. The downregulation of CHMP7 may lead to genomic instability. A strong correlation between CHMP7 and TME immune cell infiltration has been observed, participating in the formation of suppressive TME and promoting tumor progression. The expression level of CHMP7 is significantly lower in the non-responder group of multiple chemotherapeutic agents. CHMP7 can potentially serve as a new biomarker for predicting the efficacy of tumor chemotherapy and immunotherapy. Conclusion: As a gene of interest, CHMP7 is expected to provide novel and promising targets for further treatment of patients with tumor.