Luteolin overcomes resistance to benzyl isothiocyanate-induced apoptosis in human colorectal cancer HCT-116 cells

Rieko Sakai; Shintaro Yokobe; Naomi Abe; Noriyuki Miyoshi; Yoshiyuki Murata; Yoshimasa Nakamura

Luteolin overcomes resistance to benzyl isothiocyanate-induced apoptosis in human colorectal cancer HCT-116 cells

Rieko Sakai, Shintaro Yokobe, Naomi Abe, Noriyuki Miyoshi, Yoshiyuki Murata, Yoshimasa Nakamura

Research output: Contribution to journal › Article

Abstract

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 p21^waf1/cip1, a key downstream target of p53. These results suggest the role of p21^waf1/cip1 pathway in the overcoming BITC resistance by luteolin.

Original language	English
Pages (from-to)	389-393
Number of pages	5
Journal	Journal of Food and Drug Analysis
Volume	20
Issue number	SUPPL.1
Publication status	Published - Apr 1 2012

Keywords

Apoptosis
Benzyl isothiocyanate
Caspase-3
HCT116 cells
HT-29 cells
Luteolin
P21

ASJC Scopus subject areas

Food Science
Pharmacology

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Sakai, R., Yokobe, S., Abe, N., Miyoshi, N., Murata, Y., & Nakamura, Y. (2012). Luteolin overcomes resistance to benzyl isothiocyanate-induced apoptosis in human colorectal cancer HCT-116 cells. Journal of Food and Drug Analysis, 20(SUPPL.1), 389-393.

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title = "Luteolin overcomes resistance to benzyl isothiocyanate-induced apoptosis in human colorectal cancer HCT-116 cells",

abstract = "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.",

keywords = "Apoptosis, Benzyl isothiocyanate, Caspase-3, HCT116 cells, HT-29 cells, Luteolin, P21",

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AU - Sakai, Rieko

AU - Yokobe, Shintaro

AU - Abe, Naomi

AU - Miyoshi, Noriyuki

AU - Murata, Yoshiyuki

AU - Nakamura, Yoshimasa

PY - 2012/4/1

Y1 - 2012/4/1

N2 - 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.

AB - 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.

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KW - Benzyl isothiocyanate

KW - Caspase-3

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KW - HT-29 cells

KW - Luteolin

KW - P21

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