A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Laryngeal squamous cell carcinoma cell lines show high tolerance for siRNA-mediated CDK1 knockdown
Tekijät: Bednarek Kinga, Kostrzewska-Poczekaj Magdalena, Ustaszewski Adam, Janiszewska Joanna, Kiwerska Katarzyna, Paczkowska Julia, Grenman Reidar, Giefing Maciej, Jarmuz-Szymczak Malgorzata
Kustantaja: E-CENTURY PUBLISHING CORP
Julkaisuvuosi: 2021
Journal: American Journal of Cancer Research
Tietokannassa oleva lehden nimi: AMERICAN JOURNAL OF CANCER RESEARCH
Lehden akronyymi: AM J CANCER RES
Vuosikerta: 11
Numero: 5
Aloitussivu: 2081
Lopetussivu: 2094
Sivujen määrä: 14
ISSN: 2156-6976
Verkko-osoite: http://www.ajcr.us/AJCR_V11N5.html
Rinnakkaistallenteen osoite: 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.
Ladattava julkaisu This is an electronic reprint of the original article. |  |
