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Structure Activity Relationship Study of CAPE and its Derivatives on Liver Carcinoma
Author(s) -
Nguyen Julie,
Bhave Vishakha,
Hielscher Abigail,
Wang Xinyu
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.lb679
Subject(s) - caffeic acid phenethyl ester , apoptosis , viability assay , cancer research , poly adp ribose polymerase , cancer , caffeic acid , liver cancer , hepatocellular carcinoma , cell growth , chemistry , cancer cell , survivin , pharmacology , biochemistry , biology , medicine , antioxidant , enzyme , polymerase
Globally, the sixth most common cancer and the second largest contributor to cancer mortality is malignancy of the liver. The most frequent form of liver cancer is hepatocellular carcinoma (HCC), a primary liver cancer of the parenchymal cells. Presently, there are no effective treatment options aside from liver resection and transplantation. For this reason, caffeic acid phenethyl ester (CAPE) has been proposed as a potential therapeutic candidate. CAPE, a phenolic compound found in bee propolis, is reported to have a plethora of bioactive properties including antitumor traits. The objective of this study is to elucidate the relationships between the structure of CAPE and its effect on liver cancer cell growth in addition to exploring the potential mechanism for this. Seven CAPE derivatives were examined including one novel derivative previously synthesized in our lab, fluorinated caffeic acid phenethyl ester (FCAPE). We evaluated the effect of CAPE and its derivatives on the viability and proliferation of a human HCC cell line, HepG2. Our preliminary data show that CAPE and some of its derivatives reduce the viability and inhibit the proliferation of HepG2 cells in a dose‐ and time‐dependent manner. Comparison of CAPE derivatives' structures versus their activity indicates that the catechol ring functional group is required for their inhibitory effect on HepG2 cell growth. To examine whether induction of apoptosis is responsible for the cell death, western blot was conducted to check protein expression of apoptosis‐related factors including caspase‐3 and poly‐(ADP‐ribose) polymerase (PARP). Our data show the breakdown of caspase‐3 and PARP by CAPE, suggesting that CAPE may induce apoptosis of HepG2 cells. In conclusion, our data suggest that CAPE inhibits the growth of HepG2 cells through induction of apoptosis, and this effect of CAPE requires the integrity of a catechol ring functional group in order to carry out its cytotoxic effects. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .