Next Article in Journal
Lysophosphatidic Acid Receptor 5 Contributes to Imiquimod-Induced Psoriasis-Like Lesions through NLRP3 Inflammasome Activation in Macrophages
Previous Article in Journal
RTH-149 Cell Line, a Useful Tool to Decipher Molecular Mechanisms Related to Fish Nutrition
Previous Article in Special Issue
Evidence for Overlapping and Distinct Biological Activities and Transcriptional Targets Triggered by Fibroblast Growth Factor Receptor 2b Signaling between Mid- and Early Pseudoglandular Stages of Mouse Lung Development
 
 
Search for Articles:
Title / Keyword
Author / Affiliation
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
Journals
Cells
Volume 9
Issue 8
10.3390/cells9081755
cells-logo
Submit to this Journal Review for this Journal Edit a Special Issue
► Article Menu

Article Menu

share announcement question_answer thumb_up
...
textsms
...
Article

Fibroblast Growth Factor—14 Acts as Tumor Suppressor in Lung Adenocarcinomas

by
Kati Turkowski
1,†,‡,
Frederik Herzberg
1,†,‡,
Stefan Günther
1,†,‡,
David Brunn
1,†,‡,
Andreas Weigert
2,3,
Michael Meister
4,5,†,
Thomas Muley
4,5,†,
Mark Kriegsmann
5,6,†,
Marc A. Schneider
4,7,†,
Hauke Winter
5,7,†,
Michael Thomas
5,8,†,
Friedrich Grimminger
9,†,‡,
Werner Seeger
1,9,†,‡,
Soni Savai Pullamsetti
1,9,†,‡ and
Rajkumar Savai
1,3,9,10,*,†,‡
1
Max Planck Institute for Heart and Lung Research, 61231 Bad Nauheim, Germany
2
Institute of Biochemistry I, Faculty of Medicine, Goethe University Frankfurt, 60590 Frankfurt, Germany
3
Frankfurt Cancer Institute (FCI), Goethe University, 60596 Frankfurt am Main, Germany
4
Translational Research Unit, Thoraxklinik at Heidelberg University, 69126 Heidelberg, Germany
5
Translational Lung Research Center (TLRC) Heidelberg, 69126 Heidelberg, Germany
6
Institute of Pathology, University Hospital of Heidelberg, 69126 Heidelberg, Germany
7
Department of Surgery, Thoraxklinik, University Hospital Heidelberg, 69126 Heidelberg, Germany
8
Department of Oncology, Thoraxklinik, University Hospital Heidelberg, 69126 Heidelberg, Germany
9
Department of Internal Medicine, Justus Liebig University, 35392 Giessen, Germany
10
Institute for Lung Health (ILH), Justus Liebig University, 35392 Giessen, Germany
*
Author to whom correspondence should be addressed.
†
Member of the German Center for Lung Research (DZL).
‡
Member of the Cardio-Pulmonary Institute (CPI).
Cells 2020, 9(8), 1755; https://doi.org/10.3390/cells9081755
Received: 29 June 2020 / Revised: 17 July 2020 / Accepted: 20 July 2020 / Published: 22 July 2020
(This article belongs to the Special Issue FGF Signaling in Lung Development, Homeostasis and Disease)
View Full-Text Download PDF
Browse Figures

Abstract

Investigation of the molecular dynamics in lung cancer is crucial for the development of new treatment strategies. Fibroblast growth factor (FGF) 14 belongs to the FGF family, which might play a crucial role in cancer progression. We analyzed lung adenocarcinoma (LUAC) patients samples and found that FGF14 was downregulated, correlating with reduced survival and oncogenic mutation status. FGF14 overexpression in lung cancer cell lines resulted in decreased proliferation, colony formation, and migration, as well as increased expression of epithelial markers and a decreased expression of mesenchymal markers, indicating a mesenchymal to epithelial transition in vitro. We verified these findings using small interfering RNA against FGF14 and further confirmed the suppressive effect of FGF14 in a NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ immunodeficient xenograft tumor model. Moreover, FGF14 overexpressing tumor cell RNA sequencing data suggests that genes affected by FGF14 were related to the extracellular matrix, playing a role in proliferation and migration. Notably, newly identified FGF14 target genes, adenosine deaminase RNA specific B1 (ADARB1), collagen and calcium-binding epidermal growth factor domain-containing protein 1 (CCBE1), α1 chain of collagen XI (COL11A1), and mucin 16 (MUC16) expression was negatively correlated with overall survival when FGF14 was downregulated in LUAC. These findings led us to suggest that FGF14 regulates proliferation and migration in LUAC. View Full-Text
Keywords: fibroblast growth factor 14; lung adenocarcinoma; xenograft model; lung cancer mesenchymal epithelial transition fibroblast growth factor 14; lung adenocarcinoma; xenograft model; lung cancer mesenchymal epithelial transition
►▼ Show Figures

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Supplementary Material

SciFeed

Share and Cite

MDPI and ACS Style

Turkowski, K.; Herzberg, F.; Günther, S.; Brunn, D.; Weigert, A.; Meister, M.; Muley, T.; Kriegsmann, M.; Schneider, M.A.; Winter, H.; Thomas, M.; Grimminger, F.; Seeger, W.; Savai Pullamsetti, S.; Savai, R. Fibroblast Growth Factor—14 Acts as Tumor Suppressor in Lung Adenocarcinomas. Cells 2020, 9, 1755. https://doi.org/10.3390/cells9081755

AMA Style

Turkowski K, Herzberg F, Günther S, Brunn D, Weigert A, Meister M, Muley T, Kriegsmann M, Schneider MA, Winter H, Thomas M, Grimminger F, Seeger W, Savai Pullamsetti S, Savai R. Fibroblast Growth Factor—14 Acts as Tumor Suppressor in Lung Adenocarcinomas. Cells. 2020; 9(8):1755. https://doi.org/10.3390/cells9081755

Chicago/Turabian Style

Turkowski, Kati, Frederik Herzberg, Stefan Günther, David Brunn, Andreas Weigert, Michael Meister, Thomas Muley, Mark Kriegsmann, Marc A. Schneider, Hauke Winter, Michael Thomas, Friedrich Grimminger, Werner Seeger, Soni Savai Pullamsetti, and Rajkumar Savai. 2020. "Fibroblast Growth Factor—14 Acts as Tumor Suppressor in Lung Adenocarcinomas" Cells 9, no. 8: 1755. https://doi.org/10.3390/cells9081755

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Metrics

Article Access Map by Country/Region

1
Back to TopTop