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Zyflamend Induces Apoptosis in Pancreatic Cancer cells via modulation of Endoplasmic Reticulum stress and Autophagy
Author(s) -
Puckett Dexter,
Alani Dina,
Chahed Samah,
Frankel Victoria,
Whelan Jay,
Bettaieb Ahmed
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.664.1
Subject(s) - autophagy , pancreatic cancer , endoplasmic reticulum , cancer , medicine , apoptosis , unfolded protein response , cancer research , programmed cell death , prostate cancer , colorectal cancer , cancer cell , prostate , oncology , biology , microbiology and biotechnology , biochemistry
Background Pancreatic cancer is the fourth leading cause of death in the United States with over 53,670 new cases and 80% mortality in 2017. The 5‐year relative survival rate for patients with pancreatic cancer is 8.2%. Currently available therapies have only moderate efficacy, but notable limitations. Hence, there is an urgent need for alternative therapeutic approaches. Zyflamend, touted as a natural herbal extract to treat inflammation, is credited as being able to benefit many other conditions such as cancer including oral, mammary, bone, skin, colorectal, and prostate cancer. However, its effects on pancreatic cancer in particular, remain largely unexplored. Objective The objective of this study is to investigate the effects of Zyflamend on pancreatic cancer survival and decipher the underlying molecular mechanisms Methods Pancreatic cancer cells were treated with Zyflamend and key signaling pathways involved in the survival and proliferation of cells were investigated. Results Zyflamend treatment caused a dose‐dependent decrease in cell proliferation, consistent with an increase in apoptotic cell death. The effects of Zyflamend were mediated, at least partially, through alterations in autophagy and endoplasmic reticulum stress. Conclusion These studies identify Zyflamend as a potential novel approach to treat pancreatic cancer. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .

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