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Updated: May 3, 2026

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MicroRNAs 143 and 145 may be involved in benign prostatic hyperplasia pathogenesis through regulation of target genes

Nayara I Viana1, Sabrina T Reis, Nelson G Dip

  • 1Laboratory of Medical Investigation (LIM55), University of Sao Paulo Medical School, Sao Paulo - Brazil.

The International Journal of Biological Markers
|January 30, 2014
PubMed
Abstract

Insights

This study found that miR-143 and miR-145 are overexpressed in benign prostatic hyperplasia (BPH), suggesting a role in the disease. Key target genes KRAS and MAP3K3 also showed increased expression in BPH.

Area of Science:

  • Molecular Biology
  • Urology
  • Oncology

Background:

  • Benign prostatic hyperplasia (BPH) is a common condition in aging men.
  • The molecular mechanisms underlying BPH pathogenesis are not fully understood.
  • MicroRNAs (miRNAs) play crucial roles in gene regulation and are implicated in various diseases.

Purpose of the Study:

  • To investigate the roles of miR-143 and miR-145 in BPH pathogenesis.
  • To analyze the gene and protein expression of their targets: KRAS, ERK5, MAP3K3, and MAP4K4 in BPH.

Main Methods:

  • Analysis of prostate tissue specimens from 44 BPH patients and 2 controls.
  • Quantification of miRNA and target gene expression using real-time polymerase chain reaction (qRT-PCR).
  • Assessment of protein levels via Western blotting.

Main Results:

  • miR-143 and miR-145 were overexpressed in 62.5% and 73.8% of BPH cases, respectively.
  • KRAS and MAP3K3 genes were overexpressed in BPH samples (79.4% and 61.5%).
  • Increased protein expression of KRAS and MAP3K3 was observed; ERK5 protein was more abundant in larger prostates.

Conclusions:

  • Overexpression of miR-143 and miR-145 suggests their association with BPH pathogenesis.
  • miR-145 may inhibit MAP4K4, and KRAS and MAP3K3 overexpression could also be linked to BPH.
  • Further research is needed to confirm these findings and elucidate the precise mechanisms.

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