3'UTR heterogeneity and cancer progression.

Trends Cell Biol

Cancer Science Institute of Singapore, National University of Singapore (NUS), Singapore; NUS Centre for Cancer Research, Yong Loo Lin School of Medicine, National University of Singapore, Singapore; Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Singapore. Electronic address:

Published: July 2023

AI Article Synopsis

  • Most human mRNAs can create different versions of their 3' untranslated regions (UTRs) due to processes like RNA editing, mA methylation, and alternative polyadenylation (APA), with new research showing that 3'UTR splicing is also important.
  • Various factors at both the genome and transcriptome levels influence these processes, leading to diversity in 3'UTRs which is linked to cancer.
  • Recent advancements in sequencing technology and computational analysis reveal potential interactions among these processes, suggesting that their misregulation may play a role in cancer development, highlighting the need for further research to inform new treatment strategies.

Article Abstract

The majority of human mRNAs generate alternative 3' untranslated regions (UTRs) through various processes, including RNA modifications such as RNA editing, mA methylation, and alternative polyadenylation (APA), with 3'UTR splicing as an emerging mechanism. Multiple factors, ranging from the genome to transcriptome level, regulate these processes and contribute to 3'UTR heterogeneity. Genomic variants in 3'UTR regions as well as aberrant 3'UTR processing alter the transcriptomic landscape and are associated with cancer. Increasing evidence, aided by high-resolution sequencing technologies and large-scale computational analyses, points towards potential crosstalk between these processes, whose deregulation may further contribute to cancer pathogenesis. In-depth characterization of these events will increase our appreciation of their significance and help to drive therapeutic development in this field.

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Source
http://dx.doi.org/10.1016/j.tcb.2022.10.001DOI Listing

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