Riddle of the Sphinx: Emerging Role of Transfer RNAs in Human Cancer.

Zhilin Qiu,Yi Hao,Shuai Yang,Xin Zhang,Yaoxin Lin,Shouping Xu,Yihai Chen,Guozheng Li,Qin Wang,Jiale Wu,Lei Zhang,Xinheng Wang,Lei Liu,Shipeng Ning

doi:10.3389/fphar.2021.794986

Abstract

The dysregulation of transfer RNA (tRNA) expression contributes to the diversity of proteomics, heterogeneity of cell populations, and instability of the genome, which may be related to human cancer susceptibility. However, the relationship between tRNA dysregulation and cancer susceptibility remains elusive because the landscape of cancer-associated tRNAs has not been portrayed yet. Furthermore, the molecular mechanisms of tRNAs involved in tumorigenesis and cancer progression have not been systematically understood. In this review, we detail current knowledge of cancer-related tRNAs and comprehensively summarize the basic characteristics and functions of these tRNAs, with a special focus on their role and involvement in human cancer. This review bridges the gap between tRNAs and cancer and broadens our understanding of their relationship, thus providing new insights and strategies to improve the potential clinical applications of tRNAs for cancer diagnosis and therapy.

Highlights

Cancer is one of the most complex diseases caused by multiple genetic disorders and cellular abnormalities
We comprehensively summarize the basic characteristics and functions of transfer RNAs (tRNAs), focusing on their involvement in various human cancers, breast cancer, lung cancer, and melanoma
In breast cancer cells, tRNA-derived fragments (tRFs) derived from tRNATyr, tRNAAsp, tRNAGly, and tRNAGlu can inhibit tumor progression by displacing the 3′-UTRs of multiple oncogenic transcripts from the RNA-binding protein Y-box binding protein 1 (YBX-1), reducing their stability (Goodarzi et al, 2015)

Summary

Introduction

Cancer is one of the most complex diseases caused by multiple genetic disorders and cellular abnormalities. In some cancers, the dysregulation of tRNAs can trigger the progression and proliferation of cancer cells by regulating transcription, translation, ribosome biogenesis and functioning as novel epigenetic factors.

Results

Conclusion