Knockdown of PFTK1 Expression by RNAi Inhibits the Proliferation and Invasion of Human Non-Small Lung Adenocarcinoma Cells

• Published in: Oncology research Vol. 24; no. 3; pp. 181 - 187
• Main Authors: Liu, Mei-han, Shi, Shao-min, Li, Kai, Chen, En-qi
• Format: Journal Article
• Language: English
• Published: Elmsford, NY Cognizant Communication Corporation 01.01.2016
• Subjects: Carcinoma, Non-Small-Cell Lung - genetics; Carcinoma, Non-Small-Cell Lung - metabolism; Carcinoma, Non-Small-Cell Lung - pathology; Cell Line, Tumor; Cell Movement - genetics; Cell Proliferation; Cyclin-Dependent Kinases - genetics; Epithelial-Mesenchymal Transition (emt); Epithelial-Mesenchymal Transition - genetics; Gene Expression Regulation, Neoplastic; Gene Knockdown Techniques; Humans; Invasion; Lung Neoplasms - genetics; Lung Neoplasms - metabolism; Lung Neoplasms - pathology; Non-Small Cell Lung Cancer (nsclc); Pftk1; RNA Interference; RNA, Small Interfering - genetics; Wnt Signaling Pathway
• ISSN: 0965-0407; 1555-3906
• DOI: 10.3727/096504016X14635761799038

PFTK1 (PFTAIRE protein kinase 1), also named CDK14 (cyclin-dependent kinase 14), is a member of the cell division cycle 2 (CDC2)-related protein kinase family. It is highly expressed in several malignant tumors. However, the role of PFTK1 in the progression of non-small cell lung cancer (NSCLC) is still elusive. In this study, we aimed to explore the expression and function of PFTK1 in NSCLC cells. Our results showed that PFTK1 was significantly upregulated in human NSCLC cell lines. Silencing the expression of PFTK1 inhibited the proliferation of NSCLC cells. In addition, silencing the expression of PFTK1 endowed NSCLC cells with decreased migration and invasion abilities, as well as epithelial-mesenchymal transition (EMT) progress in A549 cells. A mechanistic study showed that knockdown of PFTK1 inhibited the expression of β-catenin, cyclin D1, and c-Myc in A549 cells. In summary, we report that small interfering RNA (siRNA)-PFTK1 might inhibit the proliferation and invasion of NSCLC cells by suppressing the Wnt/β-catenin signaling pathway. Therefore, PFTK1 may represent a novel therapeutic target for the treatment of NSCLC.