A1 Refereed original research article in a scientific journal
Laryngeal squamous cell carcinoma cell lines show high tolerance for siRNA-mediated CDK1 knockdown
Authors: Bednarek Kinga, Kostrzewska-Poczekaj Magdalena, Ustaszewski Adam, Janiszewska Joanna, Kiwerska Katarzyna, Paczkowska Julia, Grenman Reidar, Giefing Maciej, Jarmuz-Szymczak Malgorzata
Publisher: E-CENTURY PUBLISHING CORP
Publication year: 2021
Journal: American Journal of Cancer Research
Journal name in source: AMERICAN JOURNAL OF CANCER RESEARCH
Journal acronym: AM J CANCER RES
Volume: 11
Issue: 5
First page : 2081
Last page: 2094
Number of pages: 14
ISSN: 2156-6976
Web address : http://www.ajcr.us/AJCR_V11N5.html
Self-archived copy’s web address: https://research.utu.fi/converis/portal/detail/Publication/58320868
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.
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