CDKL1 promotes tumor proliferation and invasion in colorectal cancer

CDKL1 is a member of the cell division cycle 2 (CDC2)-related serine threonine protein kinase family and is overexpressed in malignant tumors such as melanoma, breast cancer, and gastric cancer. This study aimed to evaluate whether CDKL1 can serve as a potential molecular target for colorectal cance...

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Bibliographic Details
Published in:OncoTargets and therapy 2017-01, Vol.10, p.1613-1624
Main Authors: Qin, Chunzhi, Ren, Li, Ji, Meiling, Lv, Shixu, Wei, Ye, Zhu, Dexiang, Lin, Qi, Xu, Pingping, Chang, Wenju, Xu, Jianmin
Format: Article
Language:English
Subjects:
Breast cancer
Cancer
Cancer therapies
Care and treatment
Cell cycle
Cell division
Colorectal cancer
Cyclin-dependent kinases
Development and progression
Gene expression
Genetic aspects
Health aspects
Hospitals
Innovations
Kinases
Molecular targeted therapy
Original Research
Pathogenesis
Phosphorylation
Phosphotransferases
Plasmids
Proteins
Retina
Retinoblastoma
Vectors (Biology)
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Summary:CDKL1 is a member of the cell division cycle 2 (CDC2)-related serine threonine protein kinase family and is overexpressed in malignant tumors such as melanoma, breast cancer, and gastric cancer. This study aimed to evaluate whether CDKL1 can serve as a potential molecular target for colorectal cancer therapy. Expression of CDKL1 in colorectal cancer tissues and cell lines was measured by immunohistochemistry and Western blot, respectively. To investigate the role of CDKL1 in colorectal cancer, CDKL1-small hairpin RNA-expressing lentivirus was constructed and infected into HCT116 and Caco2 cells. The effects of RNA interference (RNAi)-mediated CDKL1 downregulation on cell proliferation and invasion were assessed by CCK-8, colony formation, transwell, and tumorigenicity assays in nude mice. The effects of CDKL1 downregulation on cell cycle and apoptosis were analyzed by flow cytometry. Furthermore, microarray method and data analysis elucidated the molecular mechanisms underlying the phenomenon. CDKL1 protein was overexpressed in colorectal cancer tissues compared with paired normal tissues. Knockdown of CDKL1 in HCT116 and Caco2 significantly inhibited cell growth, colony formation ability, tumor invasion, and G1-S phase transition of the cell cycle. The knockdown of stimulated the upregulation of p15 and retinoblastoma protein. CDKL1 plays a vital role in tumor proliferation and invasion in colorectal cancer in vitro and in vivo and, thus, may be considered as a valuable target for therapeutic intervention.
ISSN:1178-6930
1178-6930
DOI:10.2147/OTT.S133014