Abstract
Gluconasturtiin, a glucosinolate present in watercress, is hydrolysed by myrosinase to form gluconasturtiin-isothiocyanate (GNST-ITC), which has potential chemopreventive effects; however, the underlying mechanisms of action have not been explored, mainly in human cell lines. The purpose of the study is to evaluate the cytotoxicity of GNST-ITC and to further assess its potential to induce apoptosis. GNST-ITC inhibited cell proliferation in both human hepatocarcinoma (HepG2) and human breast adenocarcinoma (MCF-7) cells with IC50 values of 7.83 µM and 5.02 µM, respectively. Morphological changes as a result of GNST-ITC-induced apoptosis showed chromatin condensation, nuclear fragmentation, and membrane blebbing. Additionally, Annexin V assay showed proportion of cells in early and late apoptosis upon exposure to GNST-ITC in a time-dependent manner. To delineate the mechanism of apoptosis, cell cycle arrest and expression of caspases were studied. GNST-ITC induced a time-dependent G2/M phase arrest, with reduction of 82% and 93% in HepG2 and MCF-7 cell lines, respectively. The same treatment also led to the subsequent expression of caspase-3/7 and -9 in both cells demonstrating mitochondrial-associated cell death. Collectively, these results reveal that GNST-ITC can inhibit cell proliferation and can induce cell death in HepG2 and MCF-7 cancer cells via apoptosis, highlighting its potential development as an anticancer agent.
Highlights
Chemoprevention is a cancer-control strategy to intervene, delay, or halt carcinogenesis by administration of naturally occurring or synthetic chemicals compounds
A decrease in cell viability was observed in both HepG2 and MCF-7 cell lines when treated with
No decrease in cell population was observed in both HepG2 and MCF-7 cell lines when treated with GNST only
Summary
Chemoprevention is a cancer-control strategy to intervene, delay, or halt carcinogenesis by administration of naturally occurring or synthetic chemicals compounds. Chemoprevention is highly regarded as a prospective anticancer approach to counteract cancer incidence and mortality [1]. Epidemiological and numerous clinical studies have provided the basis for cancer therapy via dietary resources [2,3]. Induction of apoptosis is considered one of the primary mechanisms employed by natural chemopreventive agents [4,5,6]. Programmed cell death, is a tightly regulated cellular suicide program in which individual cells are destroyed while the integrity and architecture of surrounding tissue is preserved [6]. Evasion of apoptosis is a common hallmark of cancer cells, and most current anticancer therapies are targeted to facilitate the cell death of cancer cells [7]
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