Downregulation of CDKL1 suppresses neuroblastoma cell proliferation, migration and invasion
Autor: | Jian Liu, Zefeng Kang, Weiyi Li, Shuiling Chen, Jing Cao, Congqing Zhang, Wenli Chu |
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Jazyk: | angličtina |
Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
SH-SY5Y Cell division Proliferation Apoptosis Nerve Tissue Proteins Biochemistry 03 medical and health sciences Neuroblastoma 0302 clinical medicine Cyclin D1 Downregulation and upregulation Invasion Cell Movement Cell Line Tumor Humans Neoplasm Invasiveness Viability assay lcsh:QH573-671 Protein kinase A Molecular Biology Migration Cell Proliferation Chemistry Cell growth lcsh:Cytology Cell Biology Cell cycle Cyclin-Dependent Kinases Research Letters Gene Expression Regulation Neoplastic 030104 developmental biology 030220 oncology & carcinogenesis Cancer research CDKL1 |
Zdroj: | Cellular & Molecular Biology Letters, Vol 24, Iss 1, Pp 1-11 (2019) Cellular & Molecular Biology Letters |
ISSN: | 1689-1392 1425-8153 |
DOI: | 10.1186/s11658-019-0139-z |
Popis: | Background Cyclin-dependent kinase-like 1 (CDKL1) is a member of the cell division control protein 2-related serine–threonine protein kinase family. It is known to occur in various malignant tumors, but its role in neuroblastoma (NB) remains unclear. Methods We constructed a CDKL1-silenced NB cell strain (SH-SY5Y) and used real-time PCR and western blotting to confirm the silencing. Functional analyses were performed using the MTT, colony-formation, FACS, wound-healing and transwell invasion assays. Results The expression of CDKL1 was significantly upregulated in NB tissue as compared to the adjacent normal tissue. CDKL1 knockdown significantly suppressed cell viability and colony formation ability. It also induced cell cycle G0/G1 phase arrest and apoptosis, and suppressed the migration and invasion ability of SH-SY5Y cells. CDKL1 knockdown decreased the CDK4, cyclin D1 and vimentin expression levels, and increased the caspase-3, PARP and E-cadherin expression levels in SH-SY5Y cells. Conclusions Our findings suggest that CDKL1 plays an important role in NB cell proliferation, migration and invasion. It might serve as a potential target for NB therapy. |
Databáze: | OpenAIRE |
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