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Treatment Resistant Cancers

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Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...

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Related Experiment Video

Updated: May 5, 2026

Implementation of In Vitro Drug Resistance Assays: Maximizing the Potential for Uncovering Clinically Relevant Resistance Mechanisms

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Published on: December 9, 2015

Understanding Enzalutamide-Resistance Based on a Functional Single-Cell Approach.

Changhui Xue¹, Hyun-Kyung Ko¹, Kasen Shi¹

¹Division of Oncological Sciences, Knight Cancer Institute, Oregon Health & Science University, Portland, Oregon, USA.

|April 11, 2025

Summary

A small subpopulation of prostate cancer cells with low androgen receptor (AR) expression drives resistance to enzalutamide therapy. These AR-low cells are selected and expanded by treatment, leading to castration-resistant prostate cancer (CRPC).

Keywords:

androgen receptor castration resistance enzalutamide prostate cancer single‐cell RNA‐Seq

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Last Updated: May 5, 2026

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Published on: December 9, 2015

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Prostate Organoid Cultures as Tools to Translate Genotypes and Mutational Profiles to Pharmacological Responses

Prostate Organoid Cultures as Tools to Translate Genotypes and Mutational Profiles to Pharmacological Responses

Published on: October 24, 2019

Area of Science:

Oncology
Molecular Biology
Genetics

Background:

Metastatic prostate cancer (PCa) treatment relies on anti-androgen or castration therapies.
Androgen-dependent PCa (ADPC) often develops resistance, progressing to incurable castration-resistant PCa (CRPC).
Mechanisms of CRPC emergence from ADPC remain largely unclear.

Purpose of the Study:

To investigate the transcriptional heterogeneity of ADPC cells.
To understand the response of ADPC cells to enzalutamide treatment.
To identify mechanisms of therapy resistance in prostate cancer.

Main Methods:

Single-cell RNA-sequencing (scRNA-Seq) of LNCaP cells.
Isolation of androgen receptor low/negative (ARlow/-) cell subpopulations.
In vitro and in vivo functional assays using xenograft models.
Single-nucleus RNA-Seq on xenografts.

Main Results:

A small subpopulation (~10%) of LNCaP cells expressed low or no androgen receptor (ARlow/-).
ARlow/- cells exhibited distinct transcriptional profiles and pathways associated with CRPC.
ARlow/- cells demonstrated enzalutamide resistance in vitro and in vivo.
Enzalutamide treatment selected for ARlow/- cells and de-selected AR-positive (AR+) cells in vivo.

Conclusions:

A clonal selection and expansion model explains enzalutamide resistance in PCa.
Pre-existing ARlow/- subpopulations are selected and expanded by anti-androgen therapy.
Targeting ARlow/- cells may be a strategy to overcome treatment resistance.