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Expression of cyclins E1 and E2 during mouse development and in neoplasia

Y Geng1, Q Yu, W Whoriskey

  • 1Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.

Proceedings of the National Academy of Sciences of the United States of America
|November 1, 2001
PubMed

Insights

Cyclin E1 and E2 proteins, crucial for cell cycle progression, share similar expression patterns and regulation by the retinoblastoma protein (pRB). Their similar molecular circuitry suggests coordinated roles in mammalian development and cancer.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Developmental Biology

Background:

  • Cyclin E1 and E2 are E-type cyclins regulating G(1)/S phase transition in mammalian cells.
  • Both cyclins partner with cyclin-dependent kinase 2 (CDK2) for kinase activity.
  • Their distinct in vivo functions and tissue-specific roles remain largely uncharacterized.

Purpose of the Study:

  • To investigate the in vivo expression patterns of cyclin E1 and E2 during mouse development.
  • To elucidate the regulatory mechanisms controlling cyclin E1 and E2 expression.
  • To explore the potential involvement of cyclins E1 and E2 in oncogenesis, particularly in breast cancer.

Main Methods:

  • Analysis of cyclin E1 and E2 expression during normal mouse embryonic development.
  • Examination of cyclin expression in cells and tissues deficient in retinoblastoma family proteins (pRB, p107, p130).
  • Assessment of cyclin E1 and E2 levels in Myc-driven mouse breast tumors and human mammary carcinomas.

Main Results:

  • Cyclin E1 and E2 exhibit highly similar expression patterns, localized to proliferating cells during embryonic development.
  • Expression of both cyclins is dependent on pRB and pRB-dependent E2F transcription factors, but independent of p107 and p130.
  • Cyclins E1 and E2 are highly expressed in Myc-driven mouse breast tumors, and cyclin E2 is overexpressed in human mammary carcinomas.

Conclusions:

  • Cyclin E1 and E2 expression is governed by conserved molecular circuitry involving pRB and E2F.
  • The similar regulatory mechanisms suggest coordinated functions for cyclins E1 and E2.
  • Dysregulation of these cyclins may contribute to mammary tumorigenesis.

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