Related Experiment Video
Updated: Aug 8, 2026

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
Published on: March 6, 2018
Registered report: the androgen receptor induces a distinct transcriptional program in castration-resistant prostate
Denise Chronscinski1, Srujana Cherukeri1, Fraser Tan2
1Noble Life Sciences, Inc. , Gaithersburg, MD , USA.
Abstract:
The Prostate Cancer Foundation-Movember Foundation Reproducibility Initiative (PCFMFRI) seeks to address growing concerns about reproducibility in scientific research by conducting replications of recent papers in the field of prostate cancer. This Registered Report describes the proposed replication plan of key experiments from "The Androgen Receptor Induces a Distinct Transcriptional Program in Castration-Resistant Prostate Cancer in Man" by Sharma and colleagues (2013), published in Cancer Cell in 2013. Of thousands of targets for the androgen receptor (AR), the authors elucidated a subset of 16 core genes that were consistently downregulated with castration and re-emerged with castration resistance. These 16 AR binding sites were distinct from those observed in cells in culture. The authors suggested that cellular context can have dramatic effects on downstream transcriptional regulation of AR binding sites. The present study will attempt to replicate Fig. 7C by comparing gene expression of the 16 core genes identified by Sharma and colleagues in xenograft tumor tissue compared to androgen treated LNCaP cells in vitro. The Prostate Cancer Foundation-Movember Foundation Reproducibility Initiative is a collaboration between the Prostate Cancer Foundation, the Movember Initiative, and Science Exchange, and the results of the replications will be published by PeerJ.
Insights
This study replicates key findings on prostate cancer gene regulation. It compares gene expression in tumors versus cell cultures to understand androgen receptor activity in castration-resistant prostate cancer.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Reproducibility is a growing concern in scientific research.
- The Prostate Cancer Foundation-Movember Foundation Reproducibility Initiative (PCFMFRI) aims to address this by replicating key studies.
- This Registered Report details a replication of experiments from Sharma et al. (2013) concerning androgen receptor (AR) targets in prostate cancer.
Purpose of the Study:
- To replicate key experiments from Sharma et al. (2013) on AR transcriptional programs in castration-resistant prostate cancer.
- To investigate the effect of cellular context on AR binding sites and downstream transcriptional regulation.
- To compare gene expression of 16 core AR target genes in xenograft tumor tissue versus in vitro cell cultures.
Main Methods:
- Replication of Fig. 7C from Sharma et al. (2013).
- Comparison of gene expression for 16 core AR target genes.
- Analysis of gene expression in xenograft tumor tissue versus androgen-treated LNCaP cells in vitro.
Main Results:
- The study aims to replicate the identification of 16 core AR target genes.
- It will assess whether these genes are consistently downregulated with castration and re-emerge with castration resistance.
- Differences in gene expression between in vivo (xenograft) and in vitro (LNCaP cells) models will be evaluated.
Conclusions:
- The findings will contribute to understanding the reproducibility of AR transcriptional regulation in prostate cancer.
- This replication will shed light on the impact of cellular context on AR binding and gene expression.
- The results will be published by PeerJ as part of the PCFMFRI collaboration.
More Related Videos
08:36Prostate Organoid Cultures as Tools to Translate Genotypes and Mutational Profiles to Pharmacological Responses
Published on: October 24, 2019
12:13Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients
Published on: November 19, 2019
Related Concept Videos
Abnormal Proliferation
mTOR Signaling and Cancer Progression
The mTOR pathway or the...