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Updated: May 14, 2026

Laser-capture Microdissection of Human Prostatic Epithelium for RNA Analysis
07:42

Laser-capture Microdissection of Human Prostatic Epithelium for RNA Analysis

Published on: November 26, 2015

TWIST1, A novel androgen-regulated gene, is a target for NKX3-1 in prostate cancer cells

Turid Eide1, Håkon Ramberg, Carlotta Glackin

  • 1Department of Tumor Biology, Institute for Cancer Research, Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway. turid.eide@ous-hf.no.

Cancer Cell International
|February 2, 2013
PubMed
Abstract

Insights

The prostate cancer tumor suppressor NKX3-1 represses TWIST1 expression, a key gene in metastasis. This regulation is androgen-dependent, highlighting NKX3-1

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • TWIST1 is crucial for epithelial-mesenchymal transition (EMT)-mediated tumor invasion and metastasis.
  • Bone metastasis is a significant characteristic of advanced prostate cancer, affecting at least 85% of fatal cases.
  • Understanding the regulation of signaling pathways in prostate cancer metastasis is critical.

Purpose of the Study:

  • To investigate the regulatory relationship between TWIST1 and NKX3-1 in prostate cancer.
  • To elucidate the role of androgens in the regulation of TWIST1 expression via NKX3-1.

Main Methods:

  • Analysis of prostate cell lines using real-time RT-PCR.
  • Chromatin immunoprecipitation (ChIP) assays.
  • Transfection of small interfering RNAs (siRNAs) and reporter constructs.

Main Results:

  • TWIST1 is an androgen-regulated gene controlled by NKX3-1.
  • Androgens repress TWIST1 expression through NKX3-1, a prostate-specific tumor suppressor often downregulated in metastatic tumors.
  • NKX3-1 binds to the TWIST1 promoter, reducing its activity, while NKX3-1 siRNA increases endogenous TWIST1 mRNA levels.

Conclusions:

  • NKX3-1 plays a vital role in suppressing TWIST1 expression.
  • The repression of TWIST1 by NKX3-1 is functionally important in prostate cancer progression to metastatic disease.
  • This study reveals a key regulatory mechanism in prostate cancer metastasis.

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