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Related Experiment Videos

Acidic environment causes apoptosis by increasing caspase activity.

H J Park1, J C Lyons, T Ohtsubo

  • 1University of Minnesota Medical School, Department of Therapeutic Radiology--Radiation Oncology, Minneapolis 55455, USA.

British Journal of Cancer
|September 2, 1999
PubMed
Summary

Acidic environments up-regulate Bax protein, initiating caspase activation and apoptosis in leukemia cells. This process, involving ICE and CPP32 caspases, impacts tumor cell proliferation and growth.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • The tumor microenvironment can be acidic, influencing cancer cell behavior.
  • Acidic conditions are known to affect cellular processes, including cell death pathways.

Purpose of the Study:

  • To investigate the molecular mechanisms by which acidic stress induces apoptosis in HL-60 human promyelocytic leukemia cells.
  • To elucidate the role of Bax protein and specific caspases (ICE and CPP32) in acid-induced apoptosis.

Main Methods:

  • Exposure of HL-60 cells to acidic media (pH 6.2-6.6).
  • Analysis of Bax protein expression, PARP cleavage, and DNA fragmentation.
  • Use of caspase inhibitors (ICE and CPP32 inhibitors).
  • Flow cytometry to assess cell cycle distribution and apoptosis.

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Main Results:

  • Acidic media rapidly increased Bax protein expression in HL-60 cells.
  • Apoptosis, indicated by PARP cleavage and DNA fragmentation, occurred after prolonged acid exposure.
  • Caspase inhibitors (ICE and CPP32) effectively suppressed acid-induced apoptosis.
  • Acidic stress-induced apoptosis predominantly occurred in G1 phase cells.

Conclusions:

  • Acidic stress triggers apoptosis in leukemia cells via Bax up-regulation and subsequent caspase activation (ICE and CPP32).
  • The findings suggest a mechanism where Bax activation leads to caspases, causing DNA damage and cell death.
  • The acidic tumor microenvironment may significantly disrupt tumor cell proliferation and growth.