期刊
BIOMEDICINE & PHARMACOTHERAPY
卷 103, 期 -, 页码 399-405出版社
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2018.04.080
关键词
Lung cancer; NSCLC; Cyclin-dependent kinase 16; CDK16; Cyclin-dependent kinase inhibitor 1B
资金
- Key Program of Natural Science Research of Higher Education of Anhui Province [KJ2017A241, KJ2016A472]
- Key Program for Excellent Young Talent in College & University of Anhui Province [gxyq2D2016168]
- National Natural Science Foundation of China [81772493]
- Science and Technology Program of Anhui Province [1606c08225, 2016080503B035, 2017070503B037]
Cyclin-dependent kinase 16 (CDK16, PCTAIRE1) expression is upregulated in a wide variety of human malignancies. However, the function(s) of CDK16 in non-small cell lung cancer (NSCLC) remain unknown. Therefore, here we investigated the role of CDK16 in NSCLC. From 43 NSCLC tumors and matching healthy control lung tissues, immunohistochemistry revealed significantly greater CDK16 and phospho-p27(Ser10) staining levels in NSCLC samples relative to healthy controls. The NSCLC cell line EKVX was transfected with a control siRNA, a CDK16-siRNA, or CDK16-siRNA + p27-siRNA. We found significantly decreased proliferation levels and significantly increased apoptosis levels in CDK16-silenced NSCLC cells. However, these effects were abrogated in cells treated with both the CDK16-siRNA and the p27-siRNA. In CDK16-silenced NSCLC cells, we found upregulated p27 and downregulated phospho-p27(Ser10) protein expression but downregulated ubiquitinated p27 and ubiquitinated phospho-p27(Ser10) protein expression. Cycloheximide-treated CDK16-silenced NSCLC cells displayed a much milder reduction in p27 protein expression over time relative to untreated CDK16-silenced NSCLC cells. In summary, CDK16 is significantly upregulated in human NSCLC tumor tissue and plays an oncogenic role in NSCLC cells via promoting cell proliferation and inhibiting apoptosis in a p27-dependent manner. Moreover, CDK16 negatively regulates expression of the p27 via ubiquination and protein degradation.
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