miRNAs and androgen deprivation therapy for prostate cancer. 2021

Maria Yu Konoshenko, and Olga E Bryzgunova, and Pavel P Laktionov
Institute of Chemical Biology and Fundamental Medicine, Siberian Branch, Russian Academy of Sciences, Novosibirsk 630090, Russia. Electronic address: msol@ngs.ru.

Androgen deprivation therapy (ADT) is mainly used for the treatment of advanced, metastatic or recurrent prostate cancer (PCa). However, patients progress to ADT resistance and castration-resistant prostate cancer (CRPC) with a poor prognosis. Reliable validated markers of ADT resistance with proven clinical utility are necessary for timely correction of the therapy as well as for improvement of patient quality of life. MiRNAs involved in the ADT response and CRPC development via multiple mechanisms may act as biomarkers for patient outcomes. Available data on miRNAs associated with the ADT response (resistance and sensitivity) are summarized and analyzed in the manuscript, including analyses using bioinformatics resources. Molecular targets of miRNAs, as well as reciprocal relations between miRNAs and their targets, were studied using different databases. Special attention was dedicated to the mechanisms of ADT resistance and CRPC development, including testosterone, PI3K-AKT, VEGF pathways and associated genes. Several different approaches can be used to search for miRNAs associated with the ADT response, each of which focuses on the associated set of miRNAs - potential markers of ADT. The intersection of these approaches and combined analysis allowed us to select the most promising miRNA markers of the ADT response. Meta-analysis of the current data indicated that the selected 5 miRNAs (miRNAs - 125b, miR-21, miR-23b, miR-27b and miR-221) and 14 genes are involved in the regulation of key processes of CRPC development and represent the most promising predictors of the ADT response, further demonstrating their potential in combination therapy for advanced PCa.

UI MeSH Term Description Entries
D008297 Male Males
D011471 Prostatic Neoplasms Tumors or cancer of the PROSTATE. Cancer of Prostate,Prostate Cancer,Cancer of the Prostate,Neoplasms, Prostate,Neoplasms, Prostatic,Prostate Neoplasms,Prostatic Cancer,Cancer, Prostate,Cancer, Prostatic,Cancers, Prostate,Cancers, Prostatic,Neoplasm, Prostate,Neoplasm, Prostatic,Prostate Cancers,Prostate Neoplasm,Prostatic Cancers,Prostatic Neoplasm
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000726 Androgen Antagonists Compounds which inhibit or antagonize the biosynthesis or actions of androgens. Androgen Antagonist,Antiandrogen,Antiandrogens,Anti-Androgen Effect,Anti-Androgen Effects,Antiandrogen Effect,Antiandrogen Effects,Antagonist, Androgen,Antagonists, Androgen,Anti Androgen Effect,Anti Androgen Effects,Effect, Anti-Androgen,Effect, Antiandrogen,Effects, Anti-Androgen,Effects, Antiandrogen
D035683 MicroRNAs Small double-stranded, non-protein coding RNAs, 21-25 nucleotides in length generated from single-stranded microRNA gene transcripts by the same RIBONUCLEASE III, Dicer, that produces small interfering RNAs (RNA, SMALL INTERFERING). They become part of the RNA-INDUCED SILENCING COMPLEX and repress the translation (TRANSLATION, GENETIC) of target RNA by binding to homologous 3'UTR region as an imperfect match. The small temporal RNAs (stRNAs), let-7 and lin-4, from C. elegans, are the first 2 miRNAs discovered, and are from a class of miRNAs involved in developmental timing. RNA, Small Temporal,Small Temporal RNA,miRNA,stRNA,Micro RNA,MicroRNA,Primary MicroRNA,Primary miRNA,miRNAs,pre-miRNA,pri-miRNA,MicroRNA, Primary,RNA, Micro,Temporal RNA, Small,miRNA, Primary,pre miRNA,pri miRNA

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