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Reduced expression of ICE/caspase1 and CPP32/caspase3 in human hepatocellular carcinoma

K Fujikawa1, K Shiraki, K Sugimoto

  • 1First Department of Internal Medicine, Mie University School of Medicine, Japan.

Anticancer Research
|August 6, 2000
PubMed

Insights

Expression of key apoptosis-inducing enzymes, interleukin-1-converting enzyme (ICE)/caspase-1 and CPP32/caspase-3, is reduced in human hepatocellular carcinomas (HCCs). This downregulation, particularly of CPP32, may drive HCCs

Area of Science:

  • Molecular Biology
  • Cellular Biology
  • Oncology

Background:

  • Interleukin-1-converting enzyme (ICE)/caspase-1 and CPP32/caspase-3 are cysteine proteases crucial for apoptosis and homeostasis.
  • Human hepatocellular carcinomas (HCCs) exhibit significant resistance to apoptosis, a key process for preventing tumor development.

Purpose of the Study:

  • To investigate the expression levels of ICE and CPP32 in human HCC tissues.
  • To determine the correlation between ICE and CPP32 expression and apoptosis resistance in HCC.

Main Methods:

  • Reverse transcription PCR (RT-PCR) was used to analyze ICE and CPP32 mRNA expression in HCC tissues.
  • Immunohistochemistry was employed to assess ICE and CPP32 protein expression and localization in HCC and adjacent non-tumor tissues.
  • In situ nick end labeling (TUNEL) assay was performed to evaluate apoptosis levels.

Main Results:

  • Downregulation of both ICE and CPP32 expression was observed in HCC tissues compared to non-tumor tissues.
  • Reduced CPP32 staining intensity correlated significantly with a decreased TUNEL labeling index, indicating reduced apoptosis.
  • No significant correlation was found between ICE staining intensity and the TUNEL labeling index.

Conclusions:

  • The expression of ICE and CPP32 is significantly reduced in human HCCs.
  • The decreased expression of CPP32, in particular, may contribute to the apoptosis resistance characteristic of HCC.
  • Targeting CPP32 could be a potential therapeutic strategy for overcoming apoptosis resistance in HCC.

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