scholarly journals Curcumin enhances temsirolimus-induced apoptosis in human renal carcinoma cells through upregulation of YAP/p53

2016 ◽  
Vol 12 (6) ◽  
pp. 4999-5006 ◽  
Author(s):  
Shan Xu ◽  
Zheng Yang ◽  
Yizeng Fan ◽  
Bing Guan ◽  
Jing Jia ◽  
...  
Keyword(s):  
Renal Carcinoma ◽  
Carcinoma Cells ◽  
Induced Apoptosis ◽  
Human Renal Carcinoma ◽  
Renal Carcinoma Cells

Endoplasmic reticulum stress mediates withaferin A-induced apoptosis in human renal carcinoma cells

2011 ◽  
Vol 25 (3) ◽  
pp. 692-698 ◽  
Author(s):  
Min Jung Choi ◽  
Eun Jung Park ◽  
Kyoung Jin Min ◽  
Jong-Wook Park ◽  
Taeg Kyu Kwon
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Renal Carcinoma ◽  
Carcinoma Cells ◽  
Withaferin A ◽  
Induced Apoptosis ◽  
Human Renal Carcinoma ◽  
Renal Carcinoma Cells

scholarly journals A nitric oxide-releasing prodrug promotes apoptosis in human renal carcinoma cells: Involvement of reactive oxygen species

2021 ◽  
Vol 19 (1) ◽  
pp. 635-645
Author(s):  
Jindong Xie ◽  
Lieqian Chen ◽  
Dongqiang Huang ◽  
Weiwei Yue ◽  
Jingyu Chen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Renal Carcinoma ◽  
Reactive Oxygen ◽  
Carcinoma Cells ◽  
Oxygen Species ◽  
Induced Apoptosis ◽  
Human Renal Carcinoma ◽  
Renal Carcinoma Cells

Abstract Background JS-K is a nitric oxide (NO)-releasing prodrug of the O2-arylated diazeniumdiolate group that shows pronounced cytotoxicity and antitumor properties in numerous cancer models, including in vitro as well as in vivo. Reactive oxygen species (ROS) induce carcinogenesis by altering the redox status, causing increment in vulnerability to oxidative stress. Material and methods To determine the effect of JS-K, a glutathione S-transferase (GST)-activated NO-donor prodrug, on the induction of ROS accumulation, proliferation, and apoptosis in human renal carcinoma cells, we measured the changes of cell proliferation, apoptosis, ROS growth, and initiation of the mitochondrial signaling pathway before and after JS-K treatment. Results In vitro, dose- and time-dependent development of renal carcinoma cells were controlled for JS-K, and JS-K also triggered ROS aggregation and cell apoptosis. Treatment with JS-K induces the levels of pro-apoptotic proteins (Bak and Bax) and decrease the number of anti-apoptotic protein (Bcl-2). In fact, JS-K-induced apoptosis was reversed by the antioxidant N-acetylcysteine, and oxidized glutathione, a pro-oxidant, improved JS-K-induced apoptosis. Finally, we demonstrated that in renal carcinoma cells, JS-K improved the chemosensitivity of doxorubicin. Conclusion Our data indicate that JS-K-released NO induce apoptosis of renal carcinoma cells by increasing ROS levels.

scholarly journals Immune Check Point CD40–CD40L Activates Dendritic and Effector Cells Against Human Renal Carcinoma Cells

2019 ◽  
Vol 39 (9) ◽  
pp. 4643-4652 ◽  
Author(s):  
REGINA M. HILLEBRAND ◽  
ANNABELLE VOGT ◽  
CHRISTIAN P. STRASSBURG ◽  
MARIA A. GONZALEZ-CARMONA ◽  
INGO G.H. SCHMIDT-WOLF
Keyword(s):  
Renal Carcinoma ◽  
Carcinoma Cells ◽  
Check Point ◽  
Effector Cells ◽  
Human Renal Carcinoma ◽  
Renal Carcinoma Cells

scholarly journals Cepharanthine Enhances TRAIL-Mediated Apoptosis Through STAMBPL1-Mediated Downregulation of Survivin Expression in Renal Carcinoma Cells

2018 ◽  
Vol 19 (10) ◽  
pp. 3280 ◽  
Author(s):  
Sk Shahriyar ◽  
Seon Woo ◽  
Seung Seo ◽  
Kyoung-jin Min ◽  
Taeg Kwon
Keyword(s):  
Renal Carcinoma ◽  
Apoptotic Cell ◽  
Combined Treatment ◽  
Ectopic Expression ◽  
Survivin Expression ◽  
Carcinoma Cells ◽  
Inhibitory Protein ◽  
Anticancer Properties ◽  
Induced Apoptosis ◽  
Renal Carcinoma Cells

Cepharanthine (CEP) is a natural plant alkaloid, and has anti-inflammatory, antineoplastic, antioxidative and anticancer properties. In this study, we investigated whether CEP could sensitize renal carcinoma Caki cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis. CEP alone and TRAIL alone had no effect on apoptosis. However, combined CEP and TRAIL treatment markedly enhanced apoptotic cell death in cancer cells, but not in normal cells. CEP induced downregulation of survivin and cellular-FLICE inhibitory protein (c-FLIP) expression at post-translational levels. Ectopic expression of survivin blocked apoptosis by combined treatment with CEP plus TRAIL, but not in c-FLIP overexpression. Interestingly, CEP induced survivin downregulation through downregulation of deubiquitin protein of STAM-binding protein-like 1 (STAMBPL1). Overexpression of STAMBPL1 markedly recovered CEP-mediated survivin downregulation. Taken together, our study suggests that CEP sensitizes TRAIL-mediated apoptosis through downregulation of survivin expression at the post-translational levels in renal carcinoma cells.

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