Background
PFTK1, a novel cyclin-dependent kinase, plays pivotal roles in tumorigenesis. Cell motility and invasiveness could be enhanced by PFTK1 in various tumors. However, the function of PFTK1 in NSCLC metastasis remains unclear. In this study, the potential role of PFTK1 in NSCLC metastasis was determined. Materials and
Conclusion
In summary, PFTK1 could significantly promote lung cancer metastasis through changing EMT progress and modulating intracellular cytoskeleton F-actin expression. Taken together, our findings indicated that PFTK1 might serve as a novel therapeutic target for the inhibition of NSCLC progression.
Methods
In this study, the potential function of PFTK1 in lung cancer patients was analyzed with the Kaplan-Meier plotter database. RNA interference-mediated knockdown of PFTK1 was established in two NSCLC cell lines (H1299 and 95C) to explore the role of PFTK1 in NSCLC. The efficacy of downregulation of PFTK1 was examined by Western blot and immunofluorescence. The role of PFTK1 in cell migration and invasion ability was detected by wound healing and transwell assays. The protein levels in lung cancer cells were determined by Western blot. Immunofluorescence analysis was used to evaluate the structure of filamentous actin.
Results
Overexpression of PFTK1 was associated with the poor survival prognosis in NSCLC patients. PFTK1 knockdown cells were constructed successfully. Suppression of PFTK1 significantly inhibited the cell migration and invasion in H1299 and 95C cells. Notably, after PFTK1 downregulation, the epithelial-mesenchymal transition (EMT) markers vimentin, ZEB1 and β-catenin were obviously decreased. Additionally, immunofluorescence analysis indicated that PFTK1 downregulation remarkably induced filamentous actin depolymerization.