Myc oncogene: a key component in cell cycle regulation and its implication for lung cancer

Lung Cancer. 2001 Dec;34 Suppl 2:S43-6. doi: 10.1016/s0169-5002(01)00343-9.

Abstract

The Myc gene family which includes c-Myc, N-Myc and L-Myc, are transcription factors that play a role in cell proliferation, apoptosis and in the development of human tumors. Myc amplification and overexpression has been detected in lung cancer of different histologic subtypes. Although the mechanism of Myc action is not yet fully understood, Myc has been proposed to play a role in growth control and cell cycle progression by stimulating and repressing the expression of key cell cycle regulators. This review will focus on the role of Myc in stimulating the G1/S transition of the cell cycle by regulating the levels and activity of cyclins, cyclin dependent kinases (cdk), cdk inhibitors and the pRb-binding transcription factor E2F. It is proposed that both the overexpression of Myc and the deregulation of the pRB/E2F pathway promotes the G1 to S transition in parallel by activating cyclinE/cdk2 complexes in lung cancer cells.

Publication types

  • Review

MeSH terms

  • Apoptosis
  • Cell Cycle*
  • Cell Division
  • Cell Transformation, Neoplastic*
  • Cyclin-Dependent Kinases / biosynthesis
  • Cyclin-Dependent Kinases / pharmacology
  • Cyclins / biosynthesis
  • Cyclins / pharmacology
  • Gene Amplification*
  • Genes, myc / genetics*
  • Humans
  • Lung Neoplasms / genetics*
  • Lung Neoplasms / physiopathology*
  • Transcription Factors / biosynthesis
  • Transcription Factors / pharmacology

Substances

  • Cyclins
  • Transcription Factors
  • Cyclin-Dependent Kinases