Functions of cyclin D1 as an oncogene and regulation of cyclin D1 expression

Etsu Tashiro, Ayako Tsuchiya, Masaya Imoto

Research output: Contribution to journalArticle

182 Citations (Scopus)

Abstract

Cyclin D1 binds to the Cdk4 and Cdk6 to form a pRB kinase. Upon phosphorylation, pRB loses its repressive activity for the E2F transcription factor, which then activates transcription of several genes required for the transition from the G1- to S-phase and for DNA replication. The cyclin D1 gene is rearranged and overexpressed in centrocytic lymphomas and parathyroid tumors and it is amplified and/or overexpressed in a major fraction of human tumors of various types of cancer. Ectopic overexpression of cyclin D1 in fibroblast cultures shortens the G1 phase of the cell cycle. Furthermore, it has been demonstrated that introduction of an antisense cyclin D1 into a human carcinoma cell line, in which the cyclin D1 gene is amplified and overexpressed, causes reversion of the malignant phenotype. Thus, increased expression of cyclin D1 can play a critical role in tumor development and in maintenance of the malignant phenotype. However, it is insufficient to confer transformed properties on primary or established fibroblasts. In this review, we summarize the role of cyclin D1 on tumor development and malignant transformation. In addition, our chemical biology study to understand the regulatory mechanism of cyclin D1 transcription is also reviewed.

Original languageEnglish
Pages (from-to)629-635
Number of pages7
JournalCancer Science
Volume98
Issue number5
DOIs
Publication statusPublished - 2007 May

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Cyclin D1
Oncogenes
bcl-1 Genes
Neoplasms
Fibroblasts
E2F Transcription Factors
Phenotype
G1 Phase
DNA Replication
S Phase
Lymphoma
Cell Cycle
Phosphotransferases
Maintenance
Phosphorylation
Carcinoma
Cell Line
Genes

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Functions of cyclin D1 as an oncogene and regulation of cyclin D1 expression. / Tashiro, Etsu; Tsuchiya, Ayako; Imoto, Masaya.

In: Cancer Science, Vol. 98, No. 5, 05.2007, p. 629-635.

Research output: Contribution to journalArticle

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