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Zyflamend Induces Apoptosis in Pancreatic Cancer Cells via Modulation of the JNK Pathway
Author(s) -
Bettaieb Ahmed Bettaieb,
Puckett Dexter,
Chahed Samah,
Whelan Jay
Publication year - 2019
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.2019.33.1_supplement.lb282
Subject(s) - pancreatic cancer , apoptosis , cancer research , cancer , cancer cell , programmed cell death , in vivo , medicine , signal transduction , biology , pharmacology , microbiology and biotechnology , biochemistry
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 overall prognosis and survival rate of this diagnosis are grim, and in the vast majority of cases, terminal. Current pharmacological therapies and treatments targeting pancreatic cancer have proven ineffective far too often. Therefore, there is an urgent need for alternative therapeutic approaches. Zyflamend, an anti‐inflammatory herbal compound, has proven effective in various in‐vitro and in‐vivo cancer platforms, shows promise. However, its effects on pancreatic cancer in particular, remain largely unexplored. The objective of this study is to investigate the effects of Zyflamend on pancreatic cancer cells survival and decipher the underlying molecular mechanisms. Pancreatic cancer cells were treated with Zyflamend and key signaling pathways involved in the survival and proliferation were investigated. Our studies show that Zyflamend treatment caused a dose‐dependent decrease in cell proliferation, consistent with an increase in apoptotic cell death and activation of the JNK pathway. Additionally, Zyflamend in conjunction with chemotherapeutic compounds exhibited a synergistic effect against pancreatic cancer. Inhibition of JNK abrogated the pro‐apoptotic effects of Zyflamend. These studies identify Zyflamend as a potential novel approach to treat pancreatic cancer via modulation of the JNK pathway. Support or Funding Information This work was supported by a grant from NIH/NIDDK R00DK100736 to AB This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .