CDK4 has the ability to regulate Aurora B and Cenpp expression in mouse keratinocytes
- Sung Hyun Lee
- Liliana R.l. Rodriguez
- Rima Majumdar
- Paula L. Miliani De Marval
- Marcelo L. Rodriguez‑Puebla
Affiliations: Department of Molecular Biomedical Sciences, Center for Human Health and The Environment, North Carolina State University, Raleigh, NC 27607, USA, Department of Clinical Analysis, General Acute Hospital, Parmenio Piñeiro, Buenos Aires 1406, Argentina, Charles River Laboratories, Inc., Morrisville, NC 27560, USA
- Published online on: August 11, 2021 https://doi.org/10.3892/ol.2021.12993
Copyright: © Lee
et al. This is an open access article distributed under the
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Cyclin‑dependent kinase 4 (CDK4) is a critical molecule that regulates key aspects of cell proliferation through phosphorylation of the retinoblastoma (Rb) family of proteins. In the last few years, it has been suggested that CDK4 plays alternative roles in cell proliferation and tumorigenesis. The main aim of the present study was to define a novel CDK4 function as a transcriptional regulator of genes involved in chromosome segregation, contributing to the G2/M phase transition. Herein, chromatin‑immunoprecipitation reverse transcription‑quantitative PCR assays were performed to demonstrate that CDK4 could occupy the promoter region of genes associated with chromosomal segregation, such as Aurora‑B (Aurkb) and Centromere Protein P (CENP‑P). Moreover, gain‑ and loss‑of‑function experiments showed that CDK4 participated in the transcriptional regulation of Aurkb and CENP‑P. The finding that Aurkb may have a crucial role in chromosome bi‑orientation and the spindle assembly checkpoint, and that CENP‑P could be required for proper kinetochore function suggests that dysregulation of CDK4 expression induces chromosomal instability and, in some cases, cancer development.