# Impact of TRMT6 on prognosis and immune microenvironment in ovarian cancer

**Authors:** Jing Zhao, Xiaona Wang, Yazhuo Wang, Na Li

PMC · DOI: 10.3389/fonc.2025.1636191 · Frontiers in Oncology · 2025-10-30

## TL;DR

This study shows that the TRMT6 gene is linked to worse survival and reduced immune cell presence in ovarian cancer, suggesting it helps cancer avoid immune detection.

## Contribution

Identifies TRMT6 as an independent prognostic marker and explores its role in immune evasion in ovarian cancer.

## Key findings

- TRMT6 is significantly overexpressed in ovarian cancer and linked to poor overall survival.
- TRMT6 expression correlates with reduced infiltration of multiple immune cell types in tumors.
- TRMT6 is part of a ceRNA network involving HPSE2, miR-17-5p, and Lnc SNHG14.

## Abstract

This study investigates the impact of the m1A regulator TRMT6 on prognosis and the tumor microenvironment in ovarian cancer.

An analysis of the TCGA database was conducted, supplemented by validation from clinical specimens (13 paired samples), to systematically evaluate the expression characteristics of 10 m1A regulators. The prognostic value was assessed using the Kaplan-Meier Plotter database and Cox regression analysis. Additionally, immunohistochemistry and the Log-rank test were employed to validate the impact of TRMT6 on the prognosis and clinicopathological characteristics of ovarian cancer patients. The ssGSEA algorithm and CIBERSORT were utilized to analyze the influence of TRMT6 on the tumor immune microenvironment. We performed single-gene differential analysis of TRMT6 in the TCGA ovarian cancer database using the DESeq2 package and constructed a ceRNA network.

Three m1A regulators (TRMT10C, TRMT6, YTHDF1) were significantly overexpressed in cancer tissues (p < 0.01). Specifically, among these, TRMT6 and YTHDF1 were significantly associated with lower progression-free survival and overall survival (OS) (p < 0.01). Notably, TRMT6 emerged as an independent prognostic factor for predicting poor overall survival (HR = 2.74; 95% CI, 1.13 - 6.65; P = 0.026). TRMT6 expression had a significant correlation with the pathological stage. Furthermore, TRMT6 expression exhibited a significant negative correlation with eleven tumor-infiltrating immune cell types, including cytotoxic cells (p < 0.01). We also found that in ovarian cancer tissues with high expression of TRMT6, the enrichment scores of T cells gamma delta (p < 0.01) and Mast cells activated (p < 0.05) were significantly lower than those in tissues with low expression. HPSE2 has the most interaction nodes among mRNAs, hsa-miR-17-5p among miRNAs, and Lnc SNHG14 among lncRNAs in the ceRNA network.

The findings suggest that the m1A regulator TRMT6 may drive ovarian cancer progression by promoting immune escape.

## Linked entities

- **Genes:** TRMT6 (tRNA methyltransferase 6 non-catalytic subunit) [NCBI Gene 51605], TRMT10C (tRNA methyltransferase 10C, mitochondrial RNase P subunit) [NCBI Gene 54931], YTHDF1 (YTH N6-methyladenosine RNA binding protein F1) [NCBI Gene 54915], HPSE2 (heparanase 2 (inactive)) [NCBI Gene 60495], SNHG14 (small nucleolar RNA host gene 14) [NCBI Gene 104472715]
- **Diseases:** ovarian cancer (MONDO:0005140)

## Full-text entities

- **Genes:** TRMT6 (tRNA methyltransferase 6 non-catalytic subunit) [NCBI Gene 51605] {aka CGI-09, GCD10, Gcd10p, TRM6}, HPSE2 (heparanase 2 (inactive)) [NCBI Gene 60495] {aka HPA2, HPR2, UFS, UFS1}, SNHG14 (small nucleolar RNA host gene 14) [NCBI Gene 104472715] {aka 115HG, IC-SNURF-SNRPN, IPW, LNCAT, NCRNA00002, NCRNA00214}, TRMT10C (tRNA methyltransferase 10C, mitochondrial RNase P subunit) [NCBI Gene 54931] {aka COXPD30, HNYA, MRPP1, RG9MTD1}, YTHDF1 (YTH N6-methyladenosine RNA binding protein F1) [NCBI Gene 54915] {aka C20orf21, DF1}
- **Diseases:** cancer (MESH:D009369), ovarian cancer (MESH:D010051)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

9 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12611656/full.md

## References

51 references — full list in the complete paper: https://tomesphere.com/paper/PMC12611656/full.md

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Source: https://tomesphere.com/paper/PMC12611656