Structure Activity Relationship of CAPE and Its Derivatives on Liver Carcinoma Cells

Date of Award

5-2018

Degree Type

Thesis

Degree Name

Master of Science in Biomedical Sciences

First Advisor

Xinyu Wang, PhD

Second Advisor

Vishakha Bhave, PhD

Third Advisor

Abigail Hielscher, PhD

Fourth Advisor

Richard White, PhD, FAHA

Abstract

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 ofbioactive 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 inhibitory action of CAPE on NF-KB activation. To investigate structure activity relationship (SAR) of CAPE on liver carcinoma, 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 data show that CAPE and some of its derivatives (CAME, NOC, CA, FCAPE) reduce the viability and inhibit the proliferation of HepG2 cells in a dose- and time-dependent marmer. 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. Next, we observed that the inhibitory effect of CAPE is not through the induction of apoptosis, rather it may be due to proliferation inhibition. Lastly, we investigated whether the inhibitory effects of CAPE and its derivatives are due to the inhibition of NF-κB activation and subsequent translocation from the cytoplasm to the nucleus.

This document is currently not available here.

Share

COinS