Luteolin overcomes resistance to benzyl isothiocyanate-induced apoptosis in human colorectal cancer HCT-116 cells
We have previously identified p53, a universal sensor of genotoxic stress, as a negative regulator of the apoptosis induction by benzyl isothiocyanate (BITC) in the normal colon fibroblastoid cells. In the present study, we further confirmed that BITC has a potential to induce cytotoxicity in the p53-mutated colon cancer HT-29 cells in preference to HCT-116 cells with wild-type p53. To obtain effective induction of BITC-stimulated apoptosis in p53-positive cells, we investigated the combination effect of BITC and food ingredient that may overcome resistance to BITC. Pretreatment with luteolin potentiated the cytotoxicity induction by BITC in HCT-116 cells but not in HT-29 cells. The biochemical events related to apoptosis such as DNA ladder formation and caspase-3 activation were also enhanced by luteolin. Luteolin attenuated the expression of p21waf1/cip1, a key downstream target of p53. These results suggest the role of p21waf1/cip1 pathway in the overcoming BITC resistance by luteolin.
Sakai, R.; Yokobe, S.; Abe, N.; Miyoshi, N.; Murata, Y.; and Nakamura, Y.
"Luteolin overcomes resistance to benzyl isothiocyanate-induced apoptosis in human colorectal cancer HCT-116 cells,"
Journal of Food and Drug Analysis: Vol. 20
, Article 56.
Available at: https://doi.org/10.38212/2224-6614.2122