m6 A Regulator-Mediated Methylation Modification Patterns and Tumor Microenvironment Infiltration Characterization in Early Cervical Cancer

Background: Cervical cancer (CC) is the malignancy of female and almost cases of cervical cancer were caused by high-risk human papillomavirus (HPV) infection. Understanding the pathogenesis and characteristics of the postinfection microenvironment (PIM) in early-stage cervical cancer is needed. The mechanism of N6-methyladenosine (m 6 A) in the regulation of immune microenvironment in cervical cancer is unclear. Methods Messenger RNA (mRNA) expression profiles and clinical information of cervical cancer were downloaded from the Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) dataset GSE44001. We comprehensively evaluated the m 6 A modification patterns in early cervical cancer and systematically correlated these modification patterns with tumor microenvironment (TME) cell-infiltrating characteristics. Analysis of tumor mutational signatures and biological enrichment analysis were also conducted. Results LRPPRC had the highest mutation frequency. Writers METTL14 and ZC3H13, as well as reader YTHDF3, were prognostic risk-related genes. DEGs were significantly enriched in the C-type lectin receptor signaling pathway. The m 6 A cluster A showed a higher level of infiltration immunocytes, and the activity of most immune cells increased. The low-m 6 Sig score group was poor in prognosis compared with the high-m 6 Sig score group. Further, we found that the 23 immunocytes, excluding plasmacytoid dendritic cells, negatively correlated with the m 6 Sig score. Conclusions Dysregulation of m 6 A lays a critical foundation for understanding the regulation of early CC immunity. What’s more, evaluating the m 6 A modification pattern of early CC contributes to enhancing our knowledge of the characteristics of PIM and provides an important insight into the efficacy of HPV treatment.