Indole-3-carbinol inhibits the proliferation of colorectal carcinoma LoVo cells through activation of the apoptotic signaling pathway
- Authors
- Lee, J.Y.; Lim, H.M.; Lee, C.M.; Park, S.-H.; Nam, M.J.
- Issue Date
- Dec-2021
- Publisher
- SAGE Publications Ltd
- Keywords
- apoptosis; colon cancer; Indole-3-carbinol; LoVo cells; p53
- Citation
- HUMAN & EXPERIMENTAL TOXICOLOGY, v.40, no.12, pp.2099 - 2112
- Journal Title
- HUMAN & EXPERIMENTAL TOXICOLOGY
- Volume
- 40
- Number
- 12
- Start Page
- 2099
- End Page
- 2112
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/82860
- DOI
- 10.1177/09603271211021475
- ISSN
- 0960-3271
- Abstract
- Indole-3-carbinol (I3C) is a phytochemical that exhibits growth-inhibitory activity against various cancer cells. However, there are limited studies on the effects of I3C on colon cancer cells. In this study, the growth-inhibitory activity of I3C against the human colorectal carcinoma cell line (LoVo) was examined. The results of the 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide, colony formation, and cell counting assays revealed that I3C suppressed the proliferation of LoVo cells. Microscopy and wound-healing analyses revealed that I3C affected the morphology and inhibited the migration of LoVo cells, respectively. I3C induced apoptosis and DNA fragmentation as evidenced by the results of fluorescein isothiocyanate-conjugated annexin V staining and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling assay, respectively. Additionally, I3C arrested the cell cycle at the G0/G1 phase and enhanced the reactive oxygen species levels. Western blotting analysis revealed that treatment with I3C resulted in the activation of apoptotic proteins, such as poly(ADP-ribose) polymerase, caspase-3, caspase-7, caspase-9, Bax, Bim, and p53 in LoVo cells. These results indicate that I3C induces apoptosis in LoVo cells by upregulating p53, leading to the activation of Bax and caspases. Taken together, I3C exerts cytotoxic effects on LoVo cells by activating apoptosis. © The Author(s) 2021.
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