ArticleFrontiers in immunology2026
NTMT1 (METTL11A) promotes MYC-dependent proliferation and downstream HLA-A suppression in cervical cancer.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Identifying upstream molecular regulators linking tumor proliferation with immune-related alterations remains an important challenge in cancer therapy. NTMT1 (METTL11A), a protein N-terminal methyltransferase, has been implicated in tumorigenesis; however, its role in coordinating tumor-immune interaction is poorly understood. Methods: We performed integrative single-cell RNA sequencing (GSE208653) and spatial transcriptomics (GSE208654) analyses to characterize NTMT1 expression and function in cervical cancer. Spatial deconvolution and microenvironmental co-localization analyses were used to define context-specific effects. Functional validation was conducted using RT-qPCR, Western blotting, multiplex immunofluorescence, and flow cytometry-based assays. Results: NTMT1 exhibited heterogeneous expression across epithelial and immune cell populations, with enrichment in squamous cell carcinoma. Spatial transcriptomics revealed that NTMT1-positive regions were associated with altered immune composition, including reduced macrophage and increased NK/T cell infiltration. In epithelial-enriched regions, NTMT1 expression correlated with activation of cell cycle pathways, including MYC, E2F1, CDK1, and CCNB1. Functional experiments demonstrated that NTMT1 promotes cell cycle progression via MYC upregulation. In epithelial-NK/T co-localization niches, NTMT1 was associated with modulation of antigen presentation pathways and suppression of HLA-A expression. Functionally, NTMT1 overexpression reduced IFN-γ production by CD8 Conclusion: NTMT1 was identified as a candidate regulator associated with MYC activation and HLA-A suppression. Although the precise molecular mechanism remains to be elucidated, functional experiments demonstrated that NTMT1 overexpression was accompanied by increased MYC expression, reduced HLA-A expression, enhanced cell-cycle progression, and impaired CD8
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