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Related Experiment Video

Updated: Jun 19, 2026

An Orthotopic Murine Model of Human Prostate Cancer Metastasis

An Orthotopic Murine Model of Human Prostate Cancer Metastasis

Published on: September 18, 2013

Induction of bicalutamide sensitivity in prostate cancer cells by an epigenetic Puralpha-mediated decrease in

Xiaomei Liu¹, Alejandro Gomez-Pinillos, Xiaojun Liu

¹New York University Cancer Institute and Department of Medicine, New York University School of Medicine, New York, New York 10016, USA.

|October 1, 2009

Summary

Low-dose LBH589 restores Pur-alpha binding to androgen receptor repressor sequences, down-regulating androgen receptor transcription in prostate cancer cells. This combination therapy reverses resistance to bicalutamide and apoptosis, potentially restoring hormonal response.

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Published on: March 6, 2018

Area of Science:

Oncology
Molecular Biology
Biochemistry

Background:

Androgen receptor (AR) overexpression drives resistance to apoptosis and hormone therapy in advanced prostate cancer (PC).
Decreased nuclear Pur-alpha (Puralpha) levels and loss from AR repressor sequences (ARS) are linked to AR overexpression in castration-resistant PC.
Restoring AR transcription control is crucial for overcoming treatment resistance.

Purpose of the Study:

To investigate the effect of the histone deacetylase inhibitor LBH589 on AR transcription and bicalutamide resistance in prostate cancer cells.
To elucidate the role of Pur-alpha (Puralpha) in mediating LBH589's effects on AR regulation.

Main Methods:

Cell viability (MTT), gene expression (real-time PCR), protein levels (Western blot), DNA binding (ChIP), and apoptosis (caspase 3/7 activation) were assessed.
Androgen-independent (AI) and androgen-dependent (AD) LNCaP cells were treated with LBH589 and/or bicalutamide.
Flow cytometry was used to analyze cell cycle distribution.

Main Results:

Low-dose LBH589 treatment restored nuclear Puralpha levels and its binding to ARS in AI-cells, leading to decreased AR mRNA and protein.
LBH589 treatment induced G1 cell cycle arrest and modest caspase activation in AI-cells, similar to AD-cells.
Combined LBH589 and bicalutamide treatment synergistically inhibited AI-cell growth and significantly increased caspase 3/7 activation.

Conclusions:

LBH589 effectively restores Puralpha binding to ARS, down-regulating AR transcription and reversing bicalutamide and apoptosis resistance in prostate cancer cells.
The combination of LBH589 and bicalutamide shows promise for restoring hormonal response in castration-resistant prostate cancer patients.