Knockdown of SKA1 gene inhibits cell proliferation and metastasis in human adenoid cystic carcinoma
| Autor: | Bin Zhang, Zhong hao Liu, Keyi Li, Lexin Wang, Kai Dong, Yue hua Gao, Li-juan Zhao, Hong li Yang |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Pathology medicine.medical_specialty Chromosomal Proteins Non-Histone Adenoid cystic carcinoma Down-Regulation Biology medicine.disease_cause Small hairpin RNA 03 medical and health sciences 0302 clinical medicine Cyclin D1 Cell Line Tumor medicine Humans Neoplasm Metastasis RNA Small Interfering Cyclin B1 Cell Proliferation Pharmacology Gene knockdown Lentivirus Cell Cycle Checkpoints General Medicine Cell cycle medicine.disease Carcinoma Adenoid Cystic Gene Expression Regulation Neoplastic Cyclin E1 030104 developmental biology Gene Knockdown Techniques 030220 oncology & carcinogenesis Cancer research Carcinogenesis |
| Zdroj: | Biomedicine & Pharmacotherapy. 90:8-14 |
| ISSN: | 0753-3322 |
| DOI: | 10.1016/j.biopha.2017.03.029 |
| Popis: | The spindle and kinetochore-associated complex subunit 1(SKA1) is a newly discovered gene, which has been associated with mitosis and tumorigenesis. However, its role insalivary adenoid cystic carcinoma (SACC) is still unknown, and the invasive and metastatic mechanism in SACC is still unclear. To explore the molecular mechanism of SKA1 in the process of malignant proliferation and metastasis in adenoid cystic cancer (ACC) cells, we employed lentivirus-mediated short hairpin RNA to knockdown SKA1 in SACC-83 cells. The results demonstrated that the lentivirus-mediated shRNA-targeting SKA1 lead to a significant down-regulation of SKA1 expression. Knockdown of SKA1 inhibited cell proliferation, cell invasion, migration and the cell cycle arrest. Furthermore, knockdown of SKA1 reduced the Ndc80, CDK4, Cyclin D1, Cyclin E1, Cyclin B1 and matrix metalloproteinase-9 (MMP-9) protein expression, but increased the p27 protein expression. These findings indicated that SKA1 might be a promising target for cancer gene therapy in human ACC. |
| Databáze: | OpenAIRE |
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