Ursolic acid promotes the apoptosis of cervical cancer cells by regulating endoplasmic reticulum stress

2019 ◽  
Vol 45 (4) ◽  
pp. 877-881 ◽  
Author(s):  
Jin‐Ling Guo ◽  
Teng Han ◽  
Le Bao ◽  
Xiao‐Mei Li ◽  
Jing‐Quan Ma ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cancer Cells ◽  
Ursolic Acid ◽  
Cervical Cancer Cells

Endoplasmic reticulum stress and autophagy participate in apoptosis induced by bortezomib in cervical cancer cells

2015 ◽  
Vol 38 (2) ◽  
pp. 357-365 ◽  
Author(s):  
Yudi Zhang ◽  
Changmin Bai ◽  
Dan Lu ◽  
Xia Wu ◽  
Lili Gao ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cancer Cells ◽  
Cervical Cancer Cells

scholarly journals Tocotrienols induce endoplasmic reticulum stress and apoptosis in cervical cancer cells

2016 ◽  
Vol 11 (1) ◽  
Author(s):  
Raffaella Comitato ◽  
Barbara Guantario ◽  
Guido Leoni ◽  
Kalanithi Nesaretnam ◽  
Maria Beatrice Ronci ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cancer Cells ◽  
Induce Endoplasmic Reticulum Stress ◽  
Cervical Cancer Cells

scholarly journals Synergism of ursolic acid and cisplatin promotes apoptosis and enhances growth inhibition of cervical cancer cells via suppressing NF-κB p65

Oncotarget ◽  
2017 ◽  
Vol 8 (57) ◽  
pp. 97416-97427 ◽  
Author(s):  
Lan Li ◽  
Yu Hou ◽  
Jing Yu ◽  
Yulin Lu ◽  
Li Chang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Ursolic Acid ◽  
Cervical Cancer Cells

scholarly journals Protodioscin Induces Apoptosis Through ROS-Mediated Endoplasmic Reticulum Stress via the JNK/p38 Activation Pathways in Human Cervical Cancer Cells

2018 ◽  
Vol 46 (1) ◽  
pp. 322-334 ◽  
Author(s):  
Chia-Liang Lin ◽  
Chien-Hsing Lee ◽  
Chien-Min Chen ◽  
Chun-Wen Cheng ◽  
Pei-Ni Chen ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Endoplasmic Reticulum ◽  
Cell Death ◽  
Cell Viability ◽  
Er Stress ◽  
Cancer Cells ◽  
Cervical Cancer Cells ◽  
Stress Dependent ◽  
Human Cervical Cancer Cells ◽  
Human Cervical Cancer

Background/Aims: Protodioscin (PD) is a steroidal saponin with anti-cancer effects on a number of cancer cells, but the anti-tumor effects and mechanism of action of PD on human cervical cancer cells is unclear. Methods: We determined cell viability using the MTT assay. Cell death, mitochondrial membrane potential (MMP), intracellular reactive oxygen species (ROS) generation, and endoplasmic reticulum (ER) stress were measured on a flow cytometry. Caspase activation, ER stress, and MMP-dependent apoptosis proteins in cervical cancer cells in response to PD were determined by Western blot analysis. The ability of ATF4 binding to ChIP promoter was measured using the ChIP assay. Results: We demonstrated that PD inhibits cell viability, causes a loss of mitochondrial function, and induces apoptosis, as evidenced by up-regulation of caspase-8, -3, -9, -PARP, and Bax activation, and down-regulation of Bcl-2 expression. PD was shown to induce ROS and the ER stress pathway, including GRP78, p-eIF-2α, ATF4, and CHOP. Pre-treatment with NAC, a ROS production inhibitor, significantly reduced ER stress and apoptosis-related proteins induced by PD. Transfection of GRP78/CHOP-siRNA effectively inhibited PD-induced ER stress-dependent apoptosis. Moreover, treatment with PD significantly increased p38 and JNK activation. Co-administration of a JNK inhibitor (SP600125) or p38 inhibitor (SB203580) abolished cell death and ER stress effects during PD treatment. In addition, PD induced the expression of nuclear ATF4 and CHOP, as well as the binding ability of ATF4 to the CHOP promoter. Conclusion: Our results suggest that PD is a promising therapeutic agent for the treatment of human cervical cancer.

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