Biological effects of G1 phase arrest compound, sesquicillin, in human breast cancer cell lines

Bioorg Med Chem. 2002 Oct;10(10):3129-34. doi: 10.1016/s0968-0896(02)00225-0.

Abstract

Sesquicillin, isolated from fungal fermentation broth, strongly induced G1 phase arrest in human breast cancer cells. During G1 phase arrest, the expression level of cyclin D1, cyclin A, and cyclin E was decreased, and the expression of CDK (cyclin-dependent-kinase) inhibitor, protein p21(Waf1/Cip1), was increased in a time-dependent manner in a breast cancer cell MCF-7. Interestingly, the G1 phase arrest induced by sesquicillin also occurred independently of the tumor suppressor protein, p53. Sesquicillin inhibits the proliferation of MCF-7 via G1 phase arrest in association with the induction of CDK inhibitor protein, p21(Waf1/Cip1), and the reduction of G1 phase related-cyclin proteins.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Breast Neoplasms / drug therapy
  • Breast Neoplasms / pathology*
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins / drug effects
  • Cyclins / metabolism
  • Female
  • Fungi / chemistry
  • G1 Phase / drug effects*
  • Humans
  • Naphthalenes / isolation & purification
  • Naphthalenes / pharmacology*
  • Phosphorylation / drug effects
  • Tumor Cells, Cultured
  • Tumor Suppressor Protein p53 / pharmacology

Substances

  • CDKN1A protein, human
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins
  • Naphthalenes
  • Tumor Suppressor Protein p53
  • sesquicillin