Inhibition of caspase-1 induces cell death in pancreatic carcinoma cells and potentially modulates expression levels of bcl-2 family proteins

FEBS Lett. 2001 Feb 23;491(1-2):104-8. doi: 10.1016/s0014-5793(01)02144-5.

Abstract

Caspase-1 (interleukin-1beta-converting enzyme) is reported to play an important role in the regulation of apoptosis. We investigated the inhibition of caspase-1 by the cell permeable caspase-1 inhibitor Ac-AAVALLPAVLLALLAP-YVAD.CHO in pancreatic carcinoma cells. Inhibition of caspase-1 induced a non-apoptotic/"necrotic-like" cell death in AsPC-1, BxPC-3, MiaPaCa-2 and Panc-1 cells. Expression levels of bcl-2 and bax were up-regulated in caspase-1 inhibitor-treated cells while that of bcl-x(L) remained unaltered. Our observations support our previous findings that caspase-1 is potentially involved in anti-apoptotic processes in pancreatic carcinoma.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis*
  • Blotting, Western
  • Caspase 1 / metabolism*
  • Caspase Inhibitors
  • Cell Cycle
  • DNA Fragmentation
  • Humans
  • Necrosis*
  • Oligopeptides / pharmacology
  • Pancreatic Neoplasms
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / genetics
  • Proto-Oncogene Proteins c-bcl-2 / metabolism*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Tumor Cells, Cultured
  • Up-Regulation
  • bcl-2-Associated X Protein

Substances

  • Ac-AAVALLPAVLLALLAPYVAD-CHO
  • BAX protein, human
  • Caspase Inhibitors
  • Oligopeptides
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • bcl-2-Associated X Protein
  • Caspase 1