Targeting pre-existing club-like cells in prostate cancer potentiates androgen deprivation therapy.
1/5 보강
A critical knowledge gap in prostate cancer research is understanding whether castration-tolerant progenitor-like cells that reside in treatment-naïve tumors play a direct role in therapy resistance a
APA
Baurès M, Vieira Aleixo AS, et al. (2026). Targeting pre-existing club-like cells in prostate cancer potentiates androgen deprivation therapy.. EMBO molecular medicine, 18(3), 943-978. https://doi.org/10.1038/s44321-026-00375-y
MLA
Baurès M, et al.. "Targeting pre-existing club-like cells in prostate cancer potentiates androgen deprivation therapy.." EMBO molecular medicine, vol. 18, no. 3, 2026, pp. 943-978.
PMID
41629661 ↗
Abstract 한글 요약
A critical knowledge gap in prostate cancer research is understanding whether castration-tolerant progenitor-like cells that reside in treatment-naïve tumors play a direct role in therapy resistance and tumor progression. Herein, we reveal that the castration tolerance of LSC (Lin, Sca-1, CD49f) progenitor cells, the mouse equivalent of human prostatic Club cells, arises not from intrinsic properties, but from significant transcriptional reprogramming. Utilizing single-cell RNA sequencing of LSC cells isolated from prostate-specific Pten-deficient (Pten) mice, we identify the emergence of castration-resistant LSC cells enriched in stem-like features, driven by the transcription factor FOSL1/AP-1. We demonstrate that cells exhibiting Pten LSC characteristics are prevalent in aggressive double-negative prostate cancer (DNPC) subtypes recently identified in human castration-resistant prostate cancer (CRPC). Furthermore, our findings show that the dual-targeting agents JQ-1 and CX-6258-focused on FOSL1/AP-1 and PIM kinases, respectively-effectively suppress both the progenitor properties and the growth of mouse and human DNPC surrogates in vitro and in vivo. Thus, early eradication of castration-tolerant Club-like cells presents a promising therapeutic strategy to mitigate prostate cancer progression toward CRPC.
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