Activation of death receptor, DR5 and mitochondria-mediated apoptosis by a 3,4,5-trimethoxybenzyloxy derivative in wild-type and p53 mutant colorectal cancer cell lines

Document Type

Article

Publication Date

3-1-2020

Abstract

The rationale of designing compounds containing a (3,4,5-trimethoxybenzyloxy) phenyl moiety is largely due to its potential antioxidant and cytotoxic activities. A previous study focused on its antioxidant mechanism, whereas in this study, we investigated the cytotoxicity of a series of 28 analogues and the mechanism of apoptosis of the most cytotoxic compound against wild-type (HCT-116) and p53 mutant (HT-29) colorectal cancer cell lines. The series of analogues comprise of different families, namely hydrazone, oxadiazole, thiosemicarbazides and triazoles. In the initial cytotoxicity screening, N-(3,4,5-trimethoxybenzylidene)-4-(3,4,5-trimethoxybenzyloxy) benzohydrazide, henceforth known as, P5H, was found to be most cytotoxic against human colorectal cancer cell lines (IC50 for HCT-116=11.79 mu M and HT-29=18.52 mu M). Additionally, P5H was found to have some degree of selectivity towards cancer cells compared to normal human colon cells (CCD-112 CoN). Subsequent investigation had brought insight on P5H ability to induce apoptosis in both HCT-116 and HT-29 cell lines. Cell cycle analysis showed both cell lines were arrested at the G2/M phase upon treatment. Our study concluded that P5H induced the death receptor, DR5 in HCT-116 and mitochondria-mediated apoptosis pathway in HT-29. Therefore, P5H may be a promising candidate as a chemotherapy agent against colon cancer.

Keywords

Apoptosis, Colorectal cancer, Trimethoxybenzyloxy, HCT-116, HT-29, p53

Divisions

fac_med,CHEMISTRY,pharmacy

Funders

Universiti Malaya (RP021-14AFR),Universiti Malaya (RP035-17AFR),Ministry of Education, Malaysia (FP024-2014A)

Publication Title

Naunyn-Schmiedebergs Archives of Pharmacology

Volume

393

Issue

3

Publisher

Springer

Publisher Location

ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES

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