Chrysin induces death of prostate cancer cells by inducing ROS and ER stress

2017 ◽  
Vol 232 (12) ◽  
pp. 3786-3797 ◽  
Author(s):  
Soomin Ryu ◽  
Whasun Lim ◽  
Fuller W. Bazer ◽  
Gwonhwa Song
Keyword(s):  
Prostate Cancer ◽  
Er Stress ◽  
Cancer Cells ◽  
Prostate Cancer Cells

scholarly journals Differential targeting of androgen and glucocorticoid receptors induces ER stress and apoptosis in prostate cancer cells

Cell Cycle ◽  
2012 ◽  
Vol 11 (2) ◽  
pp. 395-406 ◽  
Author(s):  
Alexander Yemelyanov ◽  
Pankaj Bhalla ◽  
Ximing Yang ◽  
Andrey Ugolkov ◽  
Kenichi Iwadate ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Er Stress ◽  
Cancer Cells ◽  
Glucocorticoid Receptors ◽  
Prostate Cancer Cells

scholarly journals Correction: Excess hepsin proteolytic activity limits oncogenic signaling and induces ER stress and autophagy in prostate cancer cells

2020 ◽  
Vol 11 (2) ◽  
Author(s):  
Ramona Willbold ◽  
Katharina Wirth ◽  
Thomas Martini ◽  
Holger Sültmann ◽  
Christian Bolenz ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Er Stress ◽  
Cancer Cells ◽  
Proteolytic Activity ◽  
Prostate Cancer Cells ◽  
Oncogenic Signaling

scholarly journals Subverting ER-Stress towards Apoptosis by Nelfinavir and Curcumin Coexposure Augments Docetaxel Efficacy in Castration Resistant Prostate Cancer Cells

PLoS ONE ◽  
2014 ◽  
Vol 9 (8) ◽  
pp. e103109 ◽  
Author(s):  
Aditi Mathur ◽  
Zakaria Y. Abd Elmageed ◽  
Xichun Liu ◽  
Mikhail L. Kostochka ◽  
Haitao Zhang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Er Stress ◽  
Cancer Cells ◽  
Castration Resistant Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Castration Resistant

scholarly journals Dissociation of NSC606985 induces atypical ER-stress and cell death in prostate cancer cells

2016 ◽  
Vol 49 (2) ◽  
pp. 529-538 ◽  
Author(s):  
Liping Wang ◽  
Pengcheng Fu ◽  
Yuan Zhao ◽  
Guo Wang ◽  
Richard Yu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Death ◽  
Er Stress ◽  
Cancer Cells ◽  
Prostate Cancer Cells

scholarly journals In vitro Anticancer Effects of JI017 on Two Prostate Cancer Cell Lines Involve Endoplasmic Reticulum Stress Mediated by Elevated Levels of Reactive Oxygen Species

2021 ◽  
Vol 12 ◽  
Author(s):  
Min Jeong Kim ◽  
Jin Mo Ku ◽  
Se Hyang Hong ◽  
Hyo In Kim ◽  
Yun Young Kwon ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Reactive Oxygen Species ◽  
Er Stress ◽  
Cancer Cells ◽  
Human Prostate ◽  
Oxygen Species ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Anticancer Effects ◽  
Upr Pathway

Prostate cancer is the second most commonly diagnosed cancer, and prostate cancer is the second most common cause of cancer death in United States men after lung cancer. Many therapies are used to treat prostate cancer, and chemotherapy is one of the most relevant treatments. However, chemotherapy has many side effects, and repeated administration of chemotherapeutic agents leads to acquired resistance. Thus, new drugs with few side effects are needed. We investigated the molecular mechanism of action of JI017 in human prostate cancer cells. We identified an endoplasmic reticulum (ER) stress pathway that depended on the reactive oxygen species (ROS) pathway and played a crucial role in JI017-induced apoptosis. We measured cell viability by the MTS assay to determine the effect of JI017. Analysis of apoptosis, mitochondrial dysfunction, and cell cycle features was performed by flow cytometry. We used western blot and RT-PCR to measure the levels of the proteins of the unfolded protein response (UPR) pathway and apoptosis markers. Immunoprecipitation assay and transfection were used to determine the expression levels of proteins interacting with the pathways influenced by JI017 in prostate cancer cells. The anticancer effects induced by JI017 were evaluated. JI017 induced cell death that regulated apoptotic molecules and caused cell cycle arrest that inhibited the proliferation of cancer cells. Moreover, JI017 generated ROS. Accumulation of ROS caused ER stress through the PERK–eIF2α–CHOP and IRE1α-CHOP pathways. Furthermore, persistent activation of the UPR pathway induced by JI017 treatment triggered mitochondrial dysfunction, including dissipation of mitochondrial membrane potential, which activated intrinsic apoptotic pathway in human prostate cancer cells. The data indicated that N-acetyl-L-cysteine diminished apoptosis. We demonstrated that JI017 induced ER stress and cell death. Anticancer properties of JI017 in prostate cancer cells and in a human prostate cancer model involved ROS-mediated ER stress. Thus, JI017 treatment provides a new strategy for chemotherapy of prostate cancer.

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