scholarly journals Combined treatment with cotylenin A and phenethyl isothiocyanate induces strong antitumor activity mainly through the induction of ferroptotic cell death in human pancreatic cancer cells

2016 ◽  
Vol 36 (2) ◽  
pp. 968-976 ◽  
Author(s):  
Takashi Kasukabe ◽  
Yoshio Honma ◽  
Junko Okabe-Kado ◽  
Yusuke Higuchi ◽  
Nobuo Kato ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Death ◽  
Antitumor Activity ◽  
Cancer Cells ◽  
Combined Treatment ◽  
Human Pancreatic Cancer ◽  
Phenethyl Isothiocyanate ◽  
Pancreatic Cancer Cells ◽  
Strong Antitumor Activity

Plumbagin, Isolated from Plumbago zeylanica, Induces Cell Death through Apoptosis in Human Pancreatic Cancer Cells

Pancreatology ◽  
2009 ◽  
Vol 9 (6) ◽  
pp. 797-809 ◽  
Author(s):  
Chien-An Chen ◽  
Hen-Hong Chang ◽  
Chung-Yu Kao ◽  
Tung-Hu Tsai ◽  
Yu-Jen Chen
Keyword(s):  
Pancreatic Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Human Pancreatic Cancer ◽  
Plumbago Zeylanica ◽  
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.

scholarly journals Romidepsin and Tamoxifen Cooperatively Induce Senescence of Pancreatic Cancer Cells Through Downregulation of FOXM1 Expression and Induction of ROS/Lipid Peroxidation

2021 ◽  
Author(s):  
Noriko Okuma ◽  
Yoshio Honma ◽  
Takeshi Urano ◽  
Kenji Tamura
Keyword(s):  
Pancreatic Cancer ◽  
Lipid Peroxidation ◽  
Cancer Cells ◽  
Combined Treatment ◽  
Human Pancreatic Cancer ◽  
Pancreatic Cancer Cells ◽  
Foxm1 Expression ◽  
Acetyl Cysteine ◽  
Siomycin A ◽  
Species Production

Abstract Although progress has been made in chemotherapeutic strategies against pancreatic cancer, overall survival has not significantly improved over the past decade. Thus, the development of better therapeutic regimens remains a high priority. Pancreatic cancer cell lines were treated with romidepsin, an inhibitor of histone deacetylase, and tamoxifen, and their effects on cell growth, signaling and gene expression were determined. Xenografts of human pancreatic cancer CFPAC1 cells were treated with romidepsin and tamoxifen to determine their effects on tumor growth. The inhibition of the growth of pancreatic cancer cells induced by romidepsin and tamoxifen was effectively reduced by N-acetyl cysteine and α-tocopherol, respectively. The combined treatment greatly induced reactive oxygen species production and mitochondrial lipid peroxidation, and these effects were prevented by N-acetyl cysteine and α-tocopherol. Tamoxifen enhanced romidepsin-induced cell senescence. FOXM1 expression was markedly downregulated in pancreatic cancer cells treated with romidepsin, and tamoxifen further reduced FOXM1 expression in cells treated with romidepsin. Siomycin A, an inhibitor of FOXM1, induced senescence in pancreatic cancer cells. Similar results were obtained in knockdown of FOXM1 expression by siRNA. Since FOXM1 is used as a prognostic marker and therapeutic target for pancreatic cancer, a combination of the clinically available drugs romidepsin and tamoxifen might be considered for the treatment of patients with pancreatic cancer.

Mechanism of Ascorbate-Induced Cell Death in Human Pancreatic Cancer Cells: Role of Bcl-2, Beclin 1 and Autophagy

Planta Medica ◽  
2015 ◽  
Vol 81 (10) ◽  
pp. 838-846 ◽  
Author(s):  
Masayuki Fukui ◽  
Noriko Yamabe ◽  
Hye-Joung Choi ◽  
Kishore Polireddy ◽  
Qi Chen ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Beclin 1 ◽  
Human Pancreatic Cancer ◽  
Pancreatic Cancer Cells
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