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Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
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Differential expression of cell cycle regulators in CDK5-dependent medullary thyroid carcinoma tumorigenesis

Karine Pozo1, Antje Hillmann1, Alexander Augustyn2,3

  • 1Department of Psychiatry, The University of Texas Southwestern Medical Center, Dallas, TX, USA.

Oncotarget
|April 23, 2015
PubMed

Insights

Aberrant cyclin-dependent kinase 5 (CDK5) activity promotes medullary thyroid carcinoma (MTC) cell proliferation by upregulating cell cycle proteins. Targeting CDK5 may offer a new therapeutic strategy for MTC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Cycle Regulation

Background:

  • Medullary thyroid carcinoma (MTC) is a neuroendocrine cancer with limited treatment options.
  • Cyclin-dependent kinase 5 (CDK5) has been implicated in MTC pathogenesis.
  • A mouse model was developed to study MTC proliferation driven by p25, an activator of CDK5.

Purpose of the Study:

  • To identify genes and proteins differentially expressed in proliferating versus arrested MTC.
  • To elucidate the role of CDK5 in MTC cell cycle regulation and proliferation.
  • To explore potential therapeutic strategies targeting CDK5 in MTC.

Main Methods:

  • Conditional overexpression of p25 in a mouse MTC model to induce proliferation.
  • Analysis of gene and protein expression in proliferating and arrested MTC.
  • Assessment of CDK5 activity and its effect on cell cycle regulators in human MTC cells.

Main Results:

  • Downstream target genes of the retinoblastoma protein, including cell cycle regulators (CDKs, cyclins, CDK inhibitors), were upregulated in MTC in a CDK5-dependent manner.
  • Reduced CDK5 activity in human MTC cells led to downregulation of these cell cycle regulators.
  • Cell cycle proteins were overexpressed in human sporadic MTC but not hereditary MTC.

Conclusions:

  • Aberrant CDK5 activity precedes cell cycle initiation in MTC.
  • CDK5 acts as a tumor-promoting factor by facilitating cell cycle protein expression.
  • Targeting CDK5 or its downstream effectors could be a viable strategy for MTC treatment.
Keywords:
Cdk5cell cyclemedullary thyroid carcinomaneuroendocrineretinoblastoma protein

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