ERBB3 methylation and immune infiltration in tumor microenvironment of cervical cancer

ERBB3, a member of the ERBB family of receptor tyrosine kinases, plays an important role in cancer, despite its lack of intrinsic carcinogenic mechanism of cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC). Research on bioinformatics methods through multi-omics, this work proves that ERBB3 gene mutation, methylation modification have extensive regulatory mechanisms on the CESC microenvironment. We found that ERBB3 is involved in carcinogenesis of cervical cancer and is not associated with its prognosis. The carcinogenic mechanism is mainly related to the suppression of the immune system between tumor infiltrating lymphocytes (TILs) and the methylation of the RNA level. Our study indicated ERBB3 is more likely to be a carcinogenic factor than a key prognostic factor for cervical cancer. Methylation of ERBB3 may work as a checkpoint immunotherapy target in CESC, DNA methylation modification of the 4480 base pair downstream of ERBB3 transcription initiation site was the highest.

Automated summary

ERBB3 gene mutation and methylation modification have extensive regulatory mechanisms on the microenvironment of cervical squamous cell carcinoma and endocervical adenocarcinoma. ERBB3 is more likely to be a carcinogenic factor rather than a prognostic factor for cervical cancer, and its carcinogenic mechanism is related to immune system suppression and RNA methylation. Methylation of ERBB3 may serve as an immunotherapy target in cervical squamous cell carcinoma and endocervical adenocarcinoma.