scholarly journals Resveratrol-Induced Downregulation of NAF-1 Enhances the Sensitivity of Pancreatic Cancer Cells to Gemcitabine via the ROS/Nrf2 Signaling Pathways

2018 ◽  
Vol 2018 ◽  
pp. 1-16 ◽  
Author(s):  
Liang Cheng ◽  
Bin Yan ◽  
Ke Chen ◽  
Zhengdong Jiang ◽  
Cancan Zhou ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Anticancer Agent ◽  
Oxygen Species ◽  
Pancreatic Cancer Cells ◽  
Ros Accumulation ◽  
Cellular Reactive Oxygen Species ◽  
Pancreatic Cancer Therapy ◽  
Mitochondrial Membrane Protein

NAF-1 (nutrient-deprivation autophagy factor-1), which is an outer mitochondrial membrane protein, is known to play important roles in calcium metabolism, antiapoptosis, and antiautophagy. Resveratrol, a natural polyphenolic compound, is considered as a potent anticancer agent. Nevertheless, the molecular mechanisms underlying the effects of resveratrol and NAF-1 and their mediation of drug resistance in pancreatic cancer remain unclear. Here, we demonstrate that resveratrol suppresses the expression of NAF-1 in pancreatic cancer cells by inducing cellular reactive oxygen species (ROS) accumulation and activating Nrf2 signaling. In addition, the knockdown of NAF-1 activates apoptosis and impedes the proliferation of pancreatic cancer cells. More importantly, the targeting of NAF-1 by resveratrol can improve the sensitivity of pancreatic cancer cells to gemcitabine. These results highlight the significance of strategies that target NAF-1, which may enhance the efficacy of gemcitabine in pancreatic cancer therapy.

scholarly journals Bitter melon juice targets molecular mechanisms underlying gemcitabine resistance in pancreatic cancer cells

2015 ◽  
Vol 46 (4) ◽  
pp. 1849-1857 ◽  
Author(s):  
RANGANATHA R. SOMASAGARA ◽  
GAGAN DEEP ◽  
SANGEETA SHROTRIYA ◽  
MANISHA PATEL ◽  
CHAPLA AGARWAL ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Bitter Melon ◽  
Gemcitabine Resistance ◽  
Pancreatic Cancer Cells

scholarly journals Tephrosin induces apoptosis of human pancreatic cancer cells through the generation of reactive oxygen species

2021 ◽  
Vol 12 (1) ◽  
pp. 270-280
Author(s):  
Jie Du ◽  
Fan Jiang ◽  
Shen-Sheng Xu ◽  
Zi-Feng Huang ◽  
Li‐Li Chen ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Reactive Oxygen ◽  
Human Pancreatic Cancer ◽  
Oxygen Species ◽  
Pancreatic Cancer Cells

scholarly journals Reactive Oxygen Species Produced by NAD(P)H Oxidase Inhibit Apoptosis in Pancreatic Cancer Cells

2004 ◽  
Vol 279 (33) ◽  
pp. 34643-34654 ◽  
Author(s):  
Eva C. Vaquero ◽  
Mouad Edderkaoui ◽  
Stephen J. Pandol ◽  
Ilya Gukovsky ◽  
Anna S. Gukovskaya
Keyword(s):  
Reactive Oxygen Species ◽  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Pancreatic Cancer Cells

scholarly journals Inhibition of Autophagy by Deguelin Sensitizes Pancreatic Cancer Cells to Doxorubicin

2016 ◽  
Author(s):  
Xiao-Dong Xu ◽  
Yan Zhao ◽  
Min Zhang ◽  
Rui-Zhi He ◽  
Xiu-Hui Shi ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Combined Treatment ◽  
Protective Role ◽  
Pancreatic Cancer Cells ◽  
Effective Therapeutic Strategy ◽  
Cancer Experience

Pancreatic cancer is the fourth most common cause of cancer mortality worldwide. Furthermore, patients with pancreatic cancer experience limited benefit from current chemotherapeutic approaches because of drug resistance. Therefore, an effective therapeutic strategy for patients with pancreatic cancer is urgently required. Deguelin is a natural chemopreventive drug that exerts potent antiproliferative activity in solid tumors by inducing cell death. However, the molecular mechanisms underlying this activity have not been fully elucidated. Here we show that deguelin blocks autophagy and induces apoptosis in pancreatic cancer cells in vitro. Autophagy induced by doxorubicin plays a protective role in pancreatic cancer cells, and suppressing autophagy by chloroquine or silencing autophagy protein 5 enhanced doxorubicin-induced cell death. Similarly, inhibition of autophagy by deguelin also chemosensitized pancreatic cancer cell lines to doxorubicin. These findings suggest that deguelin has potent anticancer effects against pancreatic cancer and potentiates the anti-cancer effects of doxorubicin. These findings provide evidence that combined treatment with deguelin and doxorubicin represents an effective strategy for treating pancreatic cancer.

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