Posttranscriptional regulation of cancer traits by HuR

Wiley Interdiscip Rev RNA. Sep-Oct 2010;1(2):214-29. doi: 10.1002/wrna.4. Epub 2010 May 6.

Abstract

Cancer-related gene expression programs are strongly influenced by posttranscriptional mechanisms. The RNA-binding protein HuR is highly abundant in many cancers. Numerous HuR-regulated mRNAs encode proteins implicated in carcinogenesis. Here, we review the collections of HuR target mRNAs that encode proteins responsible for implementing five major cancer traits. By interacting with specific mRNA subsets, HuR enhances the levels of proteins that (1) promote cell proliferation, (2) increase cell survival, (3) elevate local angiogenesis, (4) help the cancer cell evade immune recognition, and (5) facilitate cancer cell invasion and metastasis. We propose that HuR exerts a tumorigenic function by enabling these cancer phenotypes. We discuss evidence that links HuR to several specific cancers and suggests its potential usefulness in cancer diagnosis, prognosis, and therapy.

Publication types

  • Review

MeSH terms

  • Adaptive Immunity / genetics
  • Adaptive Immunity / physiology
  • Animals
  • Cell Proliferation
  • Cell Survival / genetics
  • Cell Survival / physiology
  • ELAV Proteins / genetics
  • ELAV Proteins / metabolism
  • ELAV Proteins / physiology*
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Models, Biological
  • Neoplasms / genetics*
  • Neoplasms / metabolism
  • Quantitative Trait, Heritable*
  • RNA Processing, Post-Transcriptional

Substances

  • ELAV Proteins