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Apoptosis (the 1992 Frank Rose Memorial Lecture)

A H Wyllie1

  • 1Department of Pathology, University Medical School, Edinburgh, UK.

British Journal of Cancer
|February 1, 1993
PubMed

Insights

Cell death (apoptosis) is regulated by gene expression, with oncogenes like c-myc and p53 playing key roles. Understanding these genes helps explain chemotherapy resistance and sensitivity.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • Apoptosis, a regulated form of cell death, is characterized by distinct structural features and cellular events.
  • Gene expression critically regulates apoptosis, involving oncogenes and oncosuppressor genes.

Purpose of the Study:

  • To elucidate the regulatory roles of oncogenes and oncosuppressor genes in apoptosis.
  • To investigate the bivalent regulatory function of c-myc in cell proliferation versus apoptosis.
  • To understand how oncogenes like ras and bcl-2 influence apoptosis and cell population expansion.

Main Methods:

  • Analysis of gene expression patterns related to apoptosis and cell cycle regulation.
  • Investigating the impact of growth factors and cell cycle-blocking agents on c-myc activity.
  • Examining the role of p53 in initiating apoptosis via cell cycle arrest.
  • Correlating gene expression modulation with cellular states of proliferation and apoptosis.

Main Results:

  • c-myc acts as a bivalent regulator, promoting cell proliferation with growth factors or apoptosis under deprivation.
  • Oncogenes such as ras and bcl-2 confer resistance to apoptosis, driving rapid cell population expansion.
  • The oncosuppressor gene p53 may induce apoptosis by arresting the cell cycle (G1/S phase) in c-myc-expressing cells.
  • Chemotherapy resistance and sensitivity are linked to shifts between population expansion and high-turnover states, modulated by gene expression.

Conclusions:

  • Gene expression, particularly involving c-myc, ras, bcl-2, and p53, is central to the regulation of apoptosis.
  • The interplay between proliferation and apoptosis, influenced by oncogenes and oncosuppressors, determines cellular fate.
  • Understanding these molecular mechanisms provides insights into chemotherapy response and resistance.

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