The indolic diet-derivative, 3,3′-diindolylmethane, induced apoptosis in human colon cancer cells through upregulation of NDRG1

A. Lerner, M. Grafi-Cohen, T. Napso, N. Azzam, F. Fares

Research output: Contribution to journalArticlepeer-review

Abstract

N-myc downstream regulated gene-1 participates in carcinogenesis, angiogenesis, metastases, and anticancer drug resistance. In the present study, we analyzed the expression pattern of N-myc downstream regulated gene-1 following treatment of human colonic cancer cell lines; HCT-116 (well differentiated with wild-type p53 gene) and Colo-320 (poorly differentiated with mutant p53 gene), with 3,3′-diindolylmethane, a well-established proapoptotic agent product derived from indole-3-carbinol. Treatment of Colo-320 and HCT-116 with 3,3′-diindolylmethane disclosed inhibition of cell viability in a dose-dependent manner, mediated through apoptosis induction. The increased expression of N-myc downstream regulated gene-1 was detected only in poorly differentiated colon cancer cells, Colo-320 cell line. Our results suggest that N-myc downstream regulated gene-1 expression is enhanced by 3,3′-diindolylmethane in poorly differentiated cells and followed by induction of apoptosis. 3,3′-diindolylmethane induced apoptosis may represent a new regulator of N-myc downstream regulated gene-1 in poorly differentiated colonic cancer cells.

Original languageEnglish
Article number256178
JournalJournal of Biomedicine and Biotechnology
Volume2012
DOIs
StatePublished - 2012

ASJC Scopus subject areas

  • Genetics
  • Molecular Medicine
  • Molecular Biology
  • Health, Toxicology and Mutagenesis
  • Biotechnology

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