Trmt61b, a mitochondrial RNA methyltransferase, is responsible for mitochondrial RNA N1-methyladenosine (m1A) modification [2,3,4,5,6,8]. m1A modification is a post-transcriptional modification of RNA that impacts RNA processing, structure, and function, playing pivotal roles in various biological functions and activities, especially in cancer cell invasion, proliferation, and cell cycle regulation [1,3].

Studies on Trmt61b have revealed its significance in disease. In a case-control study, the TRMT61B rs4563180 G>C polymorphism was found to significantly reduce the risk of hepatoblastoma, and this polymorphism also correlated with the expression of TRMT61B and the nearby gene PPP1CB [2]. In Chinese children, the TRMT61B gene rs4563180 G>C polymorphism was associated with a reduced susceptibility to Wilms tumor, and the C allele was significantly associated with decreased mRNA expression of the TRMT61B gene [7]. Additionally, TRMT61B protein levels are increased in tumor cell lines with an imbalanced karyotype and in different tumor types compared to control tissues, and its depletion can lead to senescence or apoptosis depending on the level of aneuploidy in melanoma cell lines, making it a potential biomarker and therapeutic target for highly aneuploid cancers [6].

In conclusion, Trmt61b is crucial for mitochondrial RNA m1A modification. Research on its gene polymorphisms and protein levels in disease models has shown its potential association with cancer susceptibility, making it a gene of interest for understanding tumorigenesis and potentially developing cancer-related diagnostic and therapeutic strategies.