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. 2023 May;39(5):429-436.
doi: 10.1051/medsci/2023058. Epub 2023 May 23.

[Prostatic luminal progenitors: From tissue regeneration to therapeutic escape]

[Article in French]
Charles Dariane  1 , Manon Baures  2 , Julien Anract  3 , Nicolas Barry Delongchamps  3 , Jacques-Emmanuel Guidotti  2 , Vincent Goffin  2
Affiliations
Free article

[Prostatic luminal progenitors: From tissue regeneration to therapeutic escape]

[Article in French]
Charles Dariane et al. Med Sci (Paris). 2023 May.
Free article

Abstract
in English, French

Inhibition of androgen signaling is the gold standard treatment of benign prostate hyperplasia and prostate cancer. Despite the initial response to these treatments, therapeutic resistance is ultimately observed in most patients. Single cell RNAseq studies have shown that castration-tolerant luminal cells share several molecular and functional features with cells identified as luminal progenitor in physiological conditions. The increased prevalence of luminal progenitor-like cells in tumor contexts might result from their intrinsic androgen-independence and from the reprogramming of differentiated luminal cells into a castration-tolerant state. Thus, it is currently hypothesized that the luminal progenitor molecular profile might constitute a functional hub for cell survival in androgen deprivation context, a prerequisite for tumor regrowth. Therapeutic intervention interfering with luminal lineage plasticity is a promising approach to prevent prostate cancer progression.

Title: Progéniteurs luminaux prostatiques - De la régénération tissulaire à la résistance thérapeutique.

Abstract: Les traitements médicaux de l’hyperplasie bénigne et du cancer de la prostate reposent essentiellement sur l’inhibition de la signalisation androgénique. Bien qu’initialement efficaces, ces traitements sont tôt ou tard confrontés à une résistance thérapeutique. Des données récentes de séquençage d’ARN sur cellules uniques montrent que les cellules luminales survivant à la déprivation androgénique dans ces contextes pathologiques présentent un profil moléculaire semblable à celui de cellules luminales progénitrices, présentes en faible quantité dans un contexte physiologique. Ce profil moléculaire pourrait constituer un hub de résistance à la castration et résulter, en partie, de la reprogrammation des cellules luminales tumorales. L’inhibition thérapeutique de cette plasticité cellulaire constitue une piste prometteuse pour limiter la progression du cancer prostatique.

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References

    1. Speakman M, Kirby R, Doyle S, Ioannou C. Burden of male lower urinary tract symptoms (LUTS) suggestive of benign prostatic hyperplasia (BPH) - focus on the UK. BJU Int 2015 ; 115 : 508–519.
    1. McConnell JD, Roehrborn CG, Bautista OM, et al. The long-term effect of doxazosin, finasteride, and combination therapy on the clinical progression of benign prostatic hyperplasia. N Engl J Med 2003 ; 349 : 2387–2398.
    1. Ploussard G, Roubaud G, Barret E, et al. French AFU Cancer Committee Guidelines - Update 2022–2024 : prostate cancer - Management of metastatic disease and castration resistance. Prog Urol 2022; 32 : 1373–419.
    1. James ND, de Bono JS, Spears MR, et al. Abiraterone for Prostate Cancer Not Previously Treated with Hormone Therapy. N Engl J Med 2017 ; 377 : 338–351.
    1. Fizazi K, Tran N, Fein L, et al. Abiraterone plus Prednisone in Metastatic, Castration-Sensitive Prostate Cancer. N Engl J Med 2017 ; 377 : 352–360.

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