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Updated: Sep 12, 2025

An In Vitro Assay to Detect tRNA-Isopentenyl Transferase Activity
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Genetic Control of tRNA-Derived Fragments Contributes to Cancer Risk

Bin Li1,2, Hanting Li1,2, Yan Li1,2

  • 1Department of Epidemiology and Biostatistics, School of Public Health, State Key Laboratory of Metabolism and Regulation in Complex Organisms, TaiKang Center for Life and Medical Sciences, Wuhan University, Wuhan, China.

Cancer Research
|August 7, 2025
PubMed

Insights

Genetic variants influencing transfer RNA-derived fragment (tRF) expression are linked to cancer risk and drug response. A specific tRF, tRF-18-HSQS52D2, suppresses colorectal cancer by targeting the oncogene POU2F1.

Area of Science:

  • Genomics
  • Molecular Biology
  • Cancer Research

Background:

  • Transfer RNA-derived fragments (tRFs) are small non-coding RNAs with emerging roles in cancer.
  • Mutations in tRNA genes can alter tRF expression and function, necessitating further investigation into tRF regulation in cancer.

Purpose of the Study:

  • To conduct a pan-cancer analysis of tRF quantitative trait loci (tRFQTLs) to understand the genetic basis of tRF expression in cancer.
  • To investigate the role of specific tRFs and their genetic regulators in cancer pathogenesis and drug response.

Main Methods:

  • Pan-cancer analysis of 16,703 genetic variants associated with tRF expression across 31 cancer types.
  • Joint analysis of GWAS data to identify colocalization between tRFQTLs and cancer risk loci.
  • Biological assays, including RNA sequencing and ChIP-seq, to elucidate molecular mechanisms.
  • Development of a comprehensive database (Cancer-tRFQTL).

Main Results:

  • tRFQTLs are enriched in cancer risk loci and explain significant cancer heritability.
  • tRFs regulated by tRFQTLs are involved in cancer-related pathways, drug response, and immune infiltration.
  • A specific tRFQTL (rs9461276) is associated with colorectal cancer (CRC) risk, with its allele increasing tRF-18-HSQS52D2 expression.
  • tRF-18-HSQS52D2 suppresses CRC phenotypes by targeting POU2F1, an oncogene that promotes proliferation via metabolic and cell cycle pathways.

Conclusions:

  • Genetic variants influencing tRF expression play a significant role in cancer heritability and pathogenesis.
  • tRFs, like tRF-18-HSQS52D2, represent potential therapeutic targets for cancer treatment.
  • The Cancer-tRFQTL database provides a valuable resource for cancer genomics and tRF research.

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