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Retinoic acid-induced HOXA5 expression is co-regulated by HuR and miR-130a

Fan Yang1, Lin Miao, Yide Mei

  • 1Hefei National Laboratory for Physical Sciences at Microscale and School of Life Sciences, University of Science and Technology of China, Hefei, Anhui, China.

Cellular Signalling
|March 27, 2013
PubMed

Insights

Retinoic acid (RA) uses post-transcriptional regulation to control HOXA5 expression in breast cancer. This involves miR-130a and HuR protein, impacting cell growth inhibition.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Gene Regulation

Background:

  • Retinoic acid (RA) is a chemopreventive agent for breast cancer.
  • HOXA5 is a critical mediator of RA-induced breast cancer cell growth inhibition.
  • The molecular mechanisms of RA-induced HOXA5 expression are not fully understood.

Purpose of the Study:

  • To elucidate the post-transcriptional regulatory mechanisms of RA-induced HOXA5 expression.
  • To investigate the roles of miR-130a and Human antigen R (HuR) in HOXA5 regulation.

Main Methods:

  • Investigated RA treatment effects on c-Myc, miR-130a, and HOXA5 levels.
  • Utilized proteasome inhibition to study c-Myc degradation.
  • Examined HuR binding to HOXA5 mRNA 3'UTR and its effect on mRNA stability.

Main Results:

  • RA treatment leads to rapid, proteasome-dependent degradation of c-Myc.
  • Decreased c-Myc levels result in reduced miR-130a, de-repressing HOXA5 translation.
  • HuR binds to HOXA5 mRNA 3'UTR, enhancing its stability and translation in response to RA.

Conclusions:

  • HOXA5 expression is regulated by both transcriptional and post-transcriptional mechanisms.
  • HuR and miR-130a dynamically control HOXA5 mRNA turnover and translation.
  • These regulatory pathways contribute to retinoic acid's breast cancer chemoprevention effects.

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