Proscillaridin A slows the prostate cancer progression through triggering the activation of endoplasmic reticulum stress.
Androgens
Animals
Apoptosis
/ drug effects
Cell Movement
/ drug effects
Disease Progression
Docetaxel
/ pharmacology
Endoplasmic Reticulum Stress
/ drug effects
Humans
Male
Mice
Neoplasm Metastasis
/ drug therapy
Proscillaridin
/ pharmacology
Prostatic Neoplasms
/ drug therapy
Prostatic Neoplasms, Castration-Resistant
/ drug therapy
Reactive Oxygen Species
/ antagonists & inhibitors
Xenograft Model Antitumor Assays
CRPC
Proscillaridin A
Prostate cancer
endoplasmic reticulum stress
Journal
Cell cycle (Georgetown, Tex.)
ISSN: 1551-4005
Titre abrégé: Cell Cycle
Pays: United States
ID NLM: 101137841
Informations de publication
Date de publication:
03 2020
03 2020
Historique:
pubmed:
6
2
2020
medline:
26
5
2021
entrez:
4
2
2020
Statut:
ppublish
Résumé
Prostate cancer (PCa) is the second commonly diagnosed malignancy in men over the world. Although androgen deprivation therapy for advanced PCa patients has significantly improved their survival, the majority of these patients eventually develop castration-resistant prostate cancer (CRPC). Proscillaridin A (Pro A), a cardiac glycoside that is clinically used to treat various heart failure diseases, has been reported to have anticancer activity in several cancers. However, whether Pro A exerts an inhibitory effect on PCa progression remains unknown. In this study, we determined possible antitumor effects of Pro A on PCa cells and demonstrated the following: firstly, Pro A selectively inhibited androgen-independent PCa (including PC3 and DU145) cell growth and induced cell apoptosis
Identifiants
pubmed: 32009541
doi: 10.1080/15384101.2020.1716484
pmc: PMC7100983
doi:
Substances chimiques
Androgens
0
Reactive Oxygen Species
0
Docetaxel
15H5577CQD
Proscillaridin
KC6BL281EN
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
541-550Références
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