scholarly journals Andrographolide sensitizes human renal carcinoma cells to TRAIL‑induced apoptosis through upregulation of death receptor 4

2020 ◽  
Author(s):  
Ran Bi ◽  
Yuyou Deng ◽  
Chao Tang ◽  
Lei Xuan ◽  
Bo Xu ◽  
...  
Keyword(s):  
Renal Carcinoma ◽  
Death Receptor ◽  
Carcinoma Cells ◽  
Induced Apoptosis ◽  
Death Receptor 4 ◽  
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 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

scholarly journals Alternol Sensitizes Renal Carcinoma Cells to TRAIL-Induced Apoptosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Yu Ren ◽  
Xue Wang ◽  
Shuaishuai Huang ◽  
Yangkai Xu ◽  
Guobin Weng ◽  
...  
Keyword(s):  
Renal Carcinoma ◽  
Death Receptor ◽  
Annexin V ◽  
Carcinoma Cells ◽  
Luciferase Assay ◽  
Ros Generation ◽  
Antiapoptotic Proteins ◽  
Induced Apoptosis ◽  
Renal Carcinoma Cells

Purpose: Tumor necrosis factor–related apoptosis-inducing ligand (TRAIL), a member of the TNF family, can selectively induce cancer cell death while sparing normal cells. However, the application of TRAIL-based antitumor therapies has been hindered due to drug resistance. Alternol is a new compound isolated from microbial fermentation that possesses antitumor activity in different tumors. In our research, we discovered that alternol can sensitize TRAIL-induced apoptosis in renal carcinoma cells (RCCs).Materials and Methods: Cytotoxic activity was measured by MTT assay. Apoptosis was probed using the PI/annexin V method. Real-time PCR and western blot were used to test the levels of mRNA and protein, respectively. Luciferase assay was used to investigate whether CHOP regulated the expression of death receptor (DR) 5 through transcription. A xenogeneic tumor transplantation model was used to evaluate the anticancer effects of alternol/TRAIL in vivo.Results: When the mechanisms were investigated, we discovered that alternol increased DR5 expression. DR5 knockdown by siRNA eliminated the enhanced effect of alternol on TRAIL-mediated apoptosis. Alternol reduced the expression of antiapoptotic proteins and increased the levels of proapoptotic proteins. Moreover, alternol increased the level of CHOP, which is necessary for the enhancing effect of alternol on TRAIL-induced apoptosis, given that downregulation of CHOP abrogated the synergistic effect. DR5 upregulation induced by alternol required the production of reactive oxygen species (ROS). Removing ROS inhibited the induction of DR5 and blocked the antiapoptotic proteins induced by alternol.Conclusion: Taken together, our research suggested that alternol increased TRAIL-mediated apoptosis via inhibiting antiapoptotic proteins and upregulating DR5 levels via ROS generation and the CHOP pathway.

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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