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

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.
AuthorsA Lerner, M Grafi-Cohen, T Napso, N Azzam, F Fares
JournalJournal of biomedicine & biotechnology (J Biomed Biotechnol) Vol. 2012 Pg. 256178 ( 2012) ISSN: 1110-7251 [Electronic] United States
PMID22187533 (Publication Type: Journal Article)
Chemical References
  • Anticarcinogenic Agents
  • Cell Cycle Proteins
  • Indoles
  • Intracellular Signaling Peptides and Proteins
  • N-myc downstream-regulated gene 1 protein
  • 3,3'-diindolylmethane
Topics
  • Anticarcinogenic Agents (pharmacology)
  • Apoptosis (drug effects)
  • Blotting, Western
  • Cell Cycle Proteins (biosynthesis, genetics, metabolism)
  • Cell Differentiation (drug effects)
  • Cell Survival (drug effects)
  • Colonic Neoplasms (drug therapy, metabolism, pathology)
  • Gene Expression Regulation, Neoplastic (drug effects)
  • HCT116 Cells
  • Humans
  • Indoles (pharmacology)
  • Intracellular Signaling Peptides and Proteins (genetics, metabolism)
  • Up-Regulation (drug effects)

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