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Open AccessArticle

Highly Expressed FOXF1 Inhibit Non-Small-Cell Lung Cancer Growth via Inducing Tumor Suppressor and G1-Phase Cell-Cycle Arrest

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Division of Oral and Maxillofacial Surgery, Department of Dentistry, Taipei Medical University Hospital, Taipei 11031, Taiwan
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School of Dental Technology, College of Oral Medicine, Taipei Medical University, Taipei 11031, Taiwan
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School of Dentistry, College of Oral Medicine, Taipei Medical University, Taipei 11031, Taiwan
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Stem Cell Research Center, College of Oral Medicine, Taipei Medical University, Taipei 11031, Taiwan
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Division of Gastroenterology and Hepatology, Department of Internal Medicine, Taipei Medical University Hospital, Taipei 11031, Taiwan
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Division of Gastroenterology and Hepatology, Department of Internal Medicine, School of Medicine, Taipei Medical University, Taipei 11031, Taiwan
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Department of Dentistry, Taipei Medical University Hospital, Taipei 11031, Taiwan
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Department of Dentistry, Taipei Medical University-Shuang Ho Hospital, New Taipei City 23561, Taiwan
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3D Global Biotech Inc., New Taipei City 22175, Taiwan
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Graduate Institute of Basic Medicine, Fu Jen Catholic University, New Taipei City 24205, Taiwan
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Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2020, 21(9), 3227; https://doi.org/10.3390/ijms21093227
Received: 12 March 2020 / Revised: 29 April 2020 / Accepted: 30 April 2020 / Published: 2 May 2020
(This article belongs to the Special Issue Molecular Pathology of Lung and Thoracic Cancers)
Cancer pathogenesis results from genetic alteration-induced high or low transcriptional programs, which become highly dependent on regulators of gene expression. However, their role in progressive regulation of non-small-cell lung cancer (NSCLC) and how these dependencies may offer opportunities for novel therapeutic options remain to be understood. Previously, we identified forkhead box F1 (FOXF1) as a reprogramming mediator which leads to stemnesss when mesenchymal stem cells fuse with lung cancer cells, and we now examine its effect on lung cancer through establishing lowly and highly expressing FOXF1 NSCLC engineered cell lines. Higher expression of FOXF1 was enabled in cell lines through lentiviral transduction, and their viability, proliferation, and anchorage-dependent growth was assessed. Flow cytometry and Western blot were used to analyze cellular percentage in cell-cycle phases and levels of cellular cyclins, respectively. In mice, tumorigenic behavior of FOXF1 was investigated. We found that FOXF1 was downregulated in lung cancer tissues and cancer cell lines. Cell proliferation and ability of migration, anchorage-independent growth, and transformation were inhibited in H441-FOXF1H and H1299-FOXF1H, with upregulated tumor suppressor p21 and suppressed cellular cyclins, leading to cell-cycle arrest at the gap 1 (G1) phase. H441-FOXF1H and H1299-FOXF1H injected mice showed reduced tumor size. Conclusively, highly expressing FOXF1 inhibited NSCLC growth via activating tumor suppressor p21 and G1 cell-cycle arrest, thus offering a potentially novel therapeutic strategy for lung cancer. View Full-Text
Keywords: FOXF1; lung cancer; cell migration, tumor suppressor; cell cycle FOXF1; lung cancer; cell migration, tumor suppressor; cell cycle
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Wu, C.-Y.; Chan, C.-H.; Dubey, N.K.; Wei, H.-J.; Lu, J.-H.; Chang, C.-C.; Cheng, H.-C.; Ou, K.-L.; Deng, W.-P. Highly Expressed FOXF1 Inhibit Non-Small-Cell Lung Cancer Growth via Inducing Tumor Suppressor and G1-Phase Cell-Cycle Arrest. Int. J. Mol. Sci. 2020, 21, 3227.

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