Colocalization of BAX with BID and VDAC-1 in nimesulide-induced apoptosis of human colon adenocarcinoma COLO 205 cells

Michat Marek Godlewski, Barbara Gajkowska, Monika Lamparska-Przybysz, Tomasz Motyl*

*Corresponding author for this work

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

Cyclooxygenase (COX)-2 inhibitors that belong to non-steroid anti-inflammatory drug family have been shown to have an apoptosis-inducing effect on neoplastic cells. In the present study the effect of nimesulide (NIM), a specific COX-2 inhibitor, on apoptosis and interactions between BCL-2 family death promoters BAX and BID and BAX and VDAC-1 were examined in human colon adenocarcinoma COLO 205 cells. Laser scanning cytometry was applied for the measurement of expression and aggregation of apoptosis-related proteins and quantitative analysis of NIM-induced apoptosis. Double-staining immunoconfocal and immunoelectron microscopy were used for subcellular colocalization of examined proteins. NIM induced apoptosis of COLO 205 cells in a dose-dependent manner. This was accompanied by: (1) a decrease in intracellular prostaglandin (PG) E2 content; (2) subcellular redistribution and aggregation of BAX and BID on organellar membranes and within the nucleus; (3) colocalization of BAX with BID and BAX with VDAC-1 on organelles; and (4) survival of cells with the highest BCL-2 aggregation. A similar pattern of subcellular redistribution and colocalization of BAX with BID and BAX with VDAC-1 suggests that BAX (in association with BID) controls the function of VDAC-1 and its permeability for apoptogenic factors released from mitochondria of COLO 205 cells stimulated to apoptosis with NIM.

Original languageEnglish
Pages (from-to)1017-1029
Number of pages13
JournalAnti-Cancer Drugs
Volume13
Issue number10
DOIs
Publication statusPublished - Nov 2002

Keywords

  • Apoptosis
  • BAX
  • BID
  • COLO 205
  • Nimesulide
  • Prostaglandin E
  • VDAC-1

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