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Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
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Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay

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Identification of a cyclin D1 network in prostate cancer that antagonizes epithelial-mesenchymal restraint

Xiaoming Ju1, Mathew C Casimiro, Michael Gormley

  • 1Authors' Affiliations: Departments of Cancer Biology, Medical Oncology, and Stem Cell Biology and Regenerative Medicine, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania.

Cancer Research
|November 28, 2013
PubMed

Insights

Cyclin D1 inactivation reduced prostate cancer cell growth. Endogenous cyclin D1 restrains tumor progression and expands prostate stem cells, indicating its prognostic value for patient outcomes.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Prostate cancer progression is poorly understood at the molecular genetic level, hindering clinical management.
  • Gene signatures offer prognostic value, but key drivers of progression remain elusive.
  • The TGF-β/BMP-SMAD4 pathway influences prostate cancer, with EMT playing a role in progression.

Purpose of the Study:

  • To investigate the role of cyclin D1 in prostate cancer progression and its association with molecular signatures.
  • To determine if cyclin D1 influences epithelial-mesenchymal transition (EMT) and stem cell populations.
  • To evaluate the prognostic significance of cyclin D1-associated gene expression in human prostate cancer.

Main Methods:

  • In vivo and in vitro studies using murine prostate and cancer cell lines to assess cyclin D1 inactivation effects.
  • Analysis of molecular signatures associated with cyclin D1 in prostate cancer.
  • Chromatin immunoprecipitation sequencing (ChIP-seq) to identify cyclin D1 targets.
  • Correlation analysis of gene signatures with patient recurrence-free survival data.

Main Results:

  • Cyclin D1 inactivation reduced cellular proliferation in both murine prostate and cancer cell lines.
  • A cyclin D1-mediated molecular signature predicted poor recurrence-free survival in prostate cancer patients (HR, 3.75; P = 0.02).
  • Endogenous cyclin D1 restrains TGF-β, Snail, Twist, and Goosecoid signaling, while promoting Wnt and ES cell gene expression and prostate stem cell expansion.

Conclusions:

  • Cyclin D1 plays a dual role in prostate cancer by restraining EMT and expanding stem cell populations.
  • The identified cyclin D1-mediated gene expression signature holds significant prognostic value for biochemical recurrence in prostate cancer.
  • Understanding cyclin D1's molecular coordination offers potential therapeutic targets for improved prostate cancer management.

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