Abstract
Colon cancer is the third most devastating cancer type in morbidity and mortality associated with severe comorbidities in developing and developed countries. Dietary supplementation of alpha-linolenic acid has a beneficial effect on intestinal dysfunction. In the present study, we processed Allium porrum (Leek) for extraction and identified the bioactive metabolites with the potential of antiproliferative effect in HT-115 (human colon carcinoma) cells. We preliminarily analyzed the cytotoxic effects of methanol, chloroform, and hexane extracts of leek on HT-115 cells. In vitro cytotoxicity assay revealed that leek methanol extract (LME) significantly prohibited cell proliferation in a dose-as well as time-dependent manner, compared with hexane and chloroform extracts of leek. We found that LME at 0.4 and 0.2 μg/mL inhibited HT-115 cell proliferation by 50% at both 24 and 48 h. Cell morphological analysis and nuclear staining indicated that 22% of cells became apoptotic and ∼4% were necrotic after treatment with 0.4 μg/mL of LME. RT-PCR and western blot analysis showed that mRNA and protein expression levels of apoptotic markers such as p53, Bax, caspase-9, and caspase-3 were up-regulated, whereas Bcl-2 was down-regulated in cells exposed with 0.4 μg/mL LME, compared with the levels in untreated control cells. Lipid peroxidation marker (LPO) was significantly elevated in LME-treated cell lysates. The activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were significantly decreased in LME-treated cell lysates when compared with control HT-115 cells. In conclusion, the observed results demonstrate that LME significantly inhibits colon cancer cell growth via the mitochondria mediated caspase-dependent apoptosis mechanism.