The comprehensive analysis of the prognostic and functional role of N-terminal methyltransferases 1 in pan-cancer

Author:

Tan Lifan1,Li Wensong1,Su Qin2

Affiliation:

1. Department of Otolaryngology, West China-Guang’an Hospital, Sichuan University, Guang’an, Sichuan, China

2. Department of Otolaryngology, The People’s Hospital of Dujiangyan, Dujiangyan, Sichuan, China

Abstract

Background NTMT1, a transfer methylase that adds methyl groups to the N-terminus of proteins, has been identified as a critical player in tumor development and progression. However, its precise function in pan-cancer is still unclear. To gain a more comprehensive understanding of its role in cancer, we performed a thorough bioinformatics analysis. Methods To conduct our analysis, we gathered data from multiple sources, including RNA sequencing and clinical data from the TCGA database, protein expression data from the UALCAN and HPA databases, and single-cell expression data from the CancerSEA database. Additionally, we utilized TISIDB to investigate the interaction between the tumor and the immune system. To assess the impact of NTMT1 on the proliferation of SNU1076 cells, we performed a CCK8 assay. We also employed cellular immunofluorescence to detect DNA damage and used flow cytometry to measure tumor cell apoptosis. Results Our analysis revealed that NTMT1 was significantly overexpressed in various types of tumors and that high levels of NTMT1 were associated with poor survival outcomes. Functional enrichment analysis indicated that NTMT1 may contribute to tumor development and progression by regulating pathways involved in cell proliferation and immune response. In addition, we found that knockdown of NTMT1 expression led to reduced cell proliferation, increased DNA damage, and enhanced apoptosis in HNSCC cells. Conclusion High expression of NTMT1 in tumors is associated with poor prognosis. The underlying regulatory mechanism of NTMT1 in cancer is complex, and it may be involved in both the promotion of tumor development and the inhibition of the tumor immune microenvironment.

Publisher

PeerJ

Subject

General Agricultural and Biological Sciences,General Biochemistry, Genetics and Molecular Biology,General Medicine,General Neuroscience

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