ArticleOncoTargets and therapy2020
Downregulation of PFTK1 Inhibits Migration and Invasion of Non-Small Cell Lung Cancer.
Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
- Methylation-modulated PFTK1 regulates gefitinib resistance via Wnt/β-catenin signaling in EGFR mutant non-small-cell lung cancer cells.Communications biology · 2024Article
- Cytoplasmic Localization Isoform of Cyclin Y Enhanced the Metastatic Ability of Lung CancerFrontiers in cell and developmental biology · 2021Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPFTK1, 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
methodsIn 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.
resultsOverexpression 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.
conclusionIn 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.
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