HuR regulates cyclin A and cyclin B1 mRNA stability during cell proliferation

EMBO J. 2000 May 15;19(10):2340-50. doi: 10.1093/emboj/19.10.2340.

Abstract

Colorectal carcinoma RKO cells expressing reduced levels of the RNA-binding protein HuR (ASHuR) displayed markedly reduced growth. In synchronous RKO populations, HuR was almost exclusively nuclear during early G(1), increasing in the cytoplasm during late G(1), S and G(2). The expression and half-life of mRNAs encoding cyclins A and B1 similarly increased during S and G(2), then declined, indicating that mRNA stabilization contributed to their cell cycle-regulated expression. In gel-shift assays using radiolabeled cyclin RNA transcripts and RKO protein extracts, only those transcripts corresponding to the 3'-untranslated regions of cyclins A and B1 formed RNA-protein complexes in a cell cycle-dependent fashion. HuR directly bound mRNAs encoding cyclins A and B1, as anti-HuR antibodies supershifted such RNA-protein complexes. Importantly, the expression and half-life of mRNAs encoding cyclins A and B1 were reduced in ASHuR RKO cells. Our results indicate that HuR may play a critical role in cell proliferation, at least in part by mediating cell cycle-dependent stabilization of mRNAs encoding cyclins A and B1.

MeSH terms

  • Antigens, Surface*
  • Cell Cycle / genetics*
  • Cell Division / genetics
  • Cyclin A / genetics*
  • Cyclin B / genetics*
  • Cyclin B1
  • ELAV Proteins
  • ELAV-Like Protein 1
  • Gene Expression Regulation, Neoplastic
  • Humans
  • RNA, Messenger / genetics*
  • RNA-Binding Proteins / genetics*
  • Transcription, Genetic
  • Tumor Cells, Cultured

Substances

  • Antigens, Surface
  • CCNB1 protein, human
  • Cyclin A
  • Cyclin B
  • Cyclin B1
  • ELAV Proteins
  • ELAV-Like Protein 1
  • ELAVL1 protein, human
  • RNA, Messenger
  • RNA-Binding Proteins