Laryngeal squamous cell carcinoma cell lines show high tolerance for siRNA-mediated CDK1 knockdown.

Autor:	Bednarek K; Institute of Human Genetics, Polish Academy of Sciences Poznan, Poland., Kostrzewska-Poczekaj M; Institute of Human Genetics, Polish Academy of Sciences Poznan, Poland., Ustaszewski A; Institute of Human Genetics, Polish Academy of Sciences Poznan, Poland., Janiszewska J; Institute of Human Genetics, Polish Academy of Sciences Poznan, Poland., Kiwerska K; Institute of Human Genetics, Polish Academy of Sciences Poznan, Poland.; Department of Tumor Pathology, Greater Poland Cancer Centre Poznan, Poland., Paczkowska J; Institute of Human Genetics, Polish Academy of Sciences Poznan, Poland., Grenman R; Department of Otorhinolaryngology, Head and Neck Surgery, Turku University Central Hospital and Turku University Turku, Finland., Giefing M; Institute of Human Genetics, Polish Academy of Sciences Poznan, Poland., Jarmuz-Szymczak M; Institute of Human Genetics, Polish Academy of Sciences Poznan, Poland.; Department of Hematology and Bone Marrow Transplantation, Poznan University of Medical Sciences Poznan, Poland.
Jazyk:	angličtina
Zdroj:	American journal of cancer research [Am J Cancer Res] 2021 May 15; Vol. 11 (5), pp. 2081-2094. Date of Electronic Publication: 2021 May 15 (Print Publication: 2021).
Abstrakt:	Alterations of the cell cycle checkpoints lead to uncontrolled cell growth and result in tumorigenesis. One of the genes essential for cell proliferation and cell cycle regulation is CDK1 . This makes it a potential target in cancer therapy. In our previous study we have shown upregulation of this gene in laryngeal squamous cell carcinoma (LSCC). Here we analyze the impact of siRNA-mediated CDK1 knockdown on cell proliferation and viability, measured with cell growth monitoring and colorimetric test (CCK8 assay), respectively. We proved that a reduction of CDK1 expression by more than 50% has no effect on these cellular processes in LSCC cell lines (n=2). Moreover, using microarrays, we analyzed global gene expression deregulation in these cell lines after CDK1 knockdown. We searched for enriched ontologies in the group of identified 137 differentially expressed genes (>2-fold change). Within this group we found 3 enriched pathways: protein binding (GO:0005515), mitotic nuclear division (GO:0007067) and transmembrane receptor protein tyrosine kinase signaling pathway (GO:0007169) and a group of 11 genes encoding proteins for which interaction with CDK1 was indicated with the use of bioinformatic tools. Among these genes we propose three: CDK6, CALD1 and FYN as potentially dependent on CDK1 . Competing Interests: None. (AJCR Copyright © 2021.)
Databáze:	MEDLINE
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