Demethylzeylasteral (T-96) initiates extrinsic apoptosis against prostate cancer cells by inducing ROS-mediated ER stress and suppressing autophagic flux
Biol. Res
; 54: 27-27, 2021. ilus, graf
Article
in English
| LILACS
| ID: biblio-1505815
Responsible library:
CL1.1
ABSTRACT
BACKGROUND:
Demethylzeylasteral (T-96) is a pharmacologically active triterpenoid monomer extracted from Tripterygium wilfordii Hook F (TWHF) that has been reported to exhibit anti-neoplastic effects against several types of cancer cells. However, the potential anti-tumour effects of T-96 against human Prostate cancer (CaP) cells and the possible underlying mechanisms have not been well studied.RESULTS:
In the current study, T-96 exerted significant cytotoxicity to CaP cells in vitro and induced cell cycle arrest at S-phase in a dose-dependent manner. Mechanistically, T-96 promoted the initiation of autophagy but inhibited autophagic flux by inducing ROS-mediated endoplasmic reticulum (ER) stress which subsequently activated the extrinsic apoptosis pathway in CaP cells. These findings implied that T-96-induced ER stress activated the caspase-dependent apoptosis pathway to inhibit proliferation of CaP cells. Moreover, we observed that T-96 enhances the sensitivity of CaP cells to the chemotherapeutic drug, cisplatin.CONCLUSIONS:
Taken together, our data demonstrated that T-96 is a novel modulator of ER stress and autophagy, and has potential therapeutic applications against CaP in the clinic.
Full text:
Available
Collection:
International databases
Database:
LILACS
Main subject:
Prostatic Neoplasms
/
Autophagy
Limits:
Humans
/
Male
Language:
English
Journal:
Biol. Res
Journal subject:
Biology
Year:
2021
Document type:
Article
Affiliation country:
China
Institution/Affiliation country:
Chongqing University of Arts and Sciences/CN