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Evaluation of Keratinocyte Proliferation on Two- and Three-dimensional Type I Collagen Substrates
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Cyclin D3 deficiency inhibits skin tumor development, but does not affect normal keratinocyte proliferation

Sung Hyun Lee1, Xian Wang2, Sun Hye Kim3

  • 1Department of Molecular Biomedical Sciences, The Center for Human Health and The Environment and The Comparative Medicine Institute, North Carolina State University, Raleigh, NC 27607, USA.

Oncology Letters
|September 21, 2017
PubMed

Insights

Cyclin D3 deficiency in mice increases apoptosis and reduces skin tumors. However, its absence can lead to increased cyclin D1, promoting malignant progression in a CDK6-overexpressing model.

Area of Science:

  • Oncology
  • Cell Biology
  • Dermatology

Background:

  • D-type cyclins are implicated in human cancers.
  • Ras-mediated skin tumorigenesis involves cyclin D1 and D2, but cyclin D3's role is unclear.

Purpose of the Study:

  • To investigate the role of cyclin D3 in skin carcinogenesis.
  • To determine if the tumor-suppressive effect of CDK6 is dependent on cyclin D3.

Main Methods:

  • Generated and analyzed a K5CDK6/cyclin D3-/- mouse model.
  • Assessed keratinocyte proliferation, apoptosis, and skin papilloma development.
  • Performed biochemical analysis of epidermal protein expression and complex formation.

Main Results:

  • Cyclin D3 ablation increased apoptosis in hair follicle bulge cells, reducing papilloma formation.
  • In K5CDK6/cyclin D3-/- mice, cyclin D3 absence led to increased cyclin D1 expression.
  • This compensatory cyclin D1 increase promoted malignant progression of skin papillomas.

Conclusions:

  • Cyclin D3 absence enhances apoptosis, acting as a defense against skin neoplasia.
  • While CDK6's tumor-suppressive role in skin is not altered by cyclin D3 absence, compensatory cyclin D1 upregulation can drive malignant progression.
Keywords:
cell cyclecyclin D3cyclin-dependent kinase 6epidermispapillomasskin

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