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 journalArticle

7 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)389-393
Number of pages5
JournalJournal of Food and Drug Analysis
Volume20
Issue numberSUPPL.1
Publication statusPublished - 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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