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bcl-2 expression is reciprocal to p53 and c-myc expression in metastatic human colorectal cancer

R A Popescu1, A Lohri, E de Kant

  • 1Division of Oncology, Kantonsspital Basle, Switzerland.

European Journal of Cancer (Oxford, England : 1990)
|December 16, 1998
PubMed

Insights

Inhibition of apoptosis by bcl-2 may promote colorectal cancer. This study found lower bcl-2 mRNA in metastatic colorectal cancer, inversely correlated with p53 and c-myc expression.

Area of Science:

  • Molecular Biology
  • Oncology
  • Gastroenterology

Background:

  • Apoptosis (programmed cell death) inhibition is implicated in cancer development.
  • The bcl-2 gene is a key inhibitor of apoptosis.
  • Gastrointestinal mucosal cells with DNA damage may evade clearance, leading to tumors.

Purpose of the Study:

  • To investigate bcl-2 mRNA expression in colorectal cancer metastases.
  • To explore the relationship between bcl-2, p53, and c-myc expression in these tumors.

Main Methods:

  • Reverse transcription-polymerase chain reaction (RT-PCR) was used to quantify bcl-2 mRNA.
  • bcl-2 mRNA expression was compared between 21 colorectal cancer metastases and normal mucosal controls.
  • Correlations between bcl-2, p53, and c-myc expression were analyzed.

Main Results:

  • Mean bcl-2 mRNA expression was significantly lower in colorectal cancer metastases (0.45 U) compared to normal controls (1 U).
  • p53 expression was inversely correlated with bcl-2 expression (P = 0.021).
  • Tumors with elevated p53 showed significantly decreased bcl-2 mRNA (mean 0.30, P = 0.0052).
  • c-myc expression was also inversely correlated with bcl-2 expression (P = 0.025).

Conclusions:

  • Decreased bcl-2 expression is a feature of metastatic colorectal cancer.
  • The inverse correlation with p53 and c-myc suggests active downregulation of bcl-2.
  • Allelic loss on chromosome 18q may contribute to reduced bcl-2, but active regulation is also indicated.

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