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Profiling of Estrogen-regulated MicroRNAs in Breast Cancer Cells
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Elevated p53 promotes the processing of miR-18a to decrease estrogen receptor-α in female hepatocellular carcinoma.

Chiao-Ling Li1, Kun-Huei Yeh, Wan-Hsin Liu

  • 1Department of Microbiology, National Taiwan University College of Medicine, Taipei, Taiwan.

International Journal of Cancer
|July 1, 2014
PubMed
Summary
This summary is machine-generated.

Elevated p53 protein promotes miR-18a maturation, downregulating estrogen receptor alpha (ERα) in female hepatitis B virus-related hepatocellular carcinoma (HCC). This pathway activation in younger patients may worsen survival.

Keywords:
estrogengenderhepatitis B virushepatocellular carcinomamicroRNAp53

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Area of Science:

  • Oncology
  • Molecular Biology
  • Hepatology

Background:

  • Estrogen pathway acts as a tumor protector in female hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC).
  • Estrogen receptor alpha (ERα) is downregulated in 60% of female HCC cases due to elevated miR-18a suppressing ERα translation.

Purpose of the Study:

  • To elucidate the mechanism behind miR-18a upregulation in female HCC.
  • To identify novel regulators of miR-18a maturation in this context.

Main Methods:

  • Analysis of 77 female HCC specimens to correlate miR-18a levels with pri- and pre-miR-18a.
  • Investigated p53 as a regulator of miR-18a processing using siRNA knockdown and overexpression.
  • Validated p53/miR-18a association in clinical HCC specimens.

Main Results:

  • miR-18a levels correlated with pre-miR-18a, indicating enhanced processing.
  • p53 was identified as a novel positive regulator of miR-18a maturation; p53 modulation altered miR-18a levels.
  • Elevated/mutant p53 and miR-18a accumulation were confirmed in HBV-related female HCC specimens.
  • The p53/miR-18a pathway was predominantly activated in younger, noncirrhotic female HCC patients, correlating with worse survival.

Conclusions:

  • Demonstrated a novel role for elevated/mutant p53 in promoting miR-18a biogenesis.
  • This mechanism leads to decreased ERα protein levels, potentially diminishing the tumor-protective estrogen pathway in female hepatocarcinogenesis.
  • The p53/miR-18a axis represents a potential therapeutic target in specific HCC patient subgroups.