Next Article in Journal
Iron as a Central Player and Promising Target in Cancer Progression
Next Article in Special Issue
Brain-Derived Neurotrophic Factor Is Required for the Neuroprotective Effect of Mifepristone on Immature Purkinje Cells in Cerebellar Slice Culture
Previous Article in Journal
CMV-Specific Immune Response—New Patients, New Insight: Central Role of Specific IgG during Infancy and Long-Lasting Immune Deficiency after Allogenic Stem Cell Transplantation
Previous Article in Special Issue
Comparison between Polybutylcyanoacrylate Nanoparticles with Either Surface-Adsorbed or Encapsulated Brain-Derived Neurotrophic Factor on the Neural Differentiation of iPSCs
Article Menu
Issue 2 (January-2) cover image

Export Article

Open AccessArticle
Int. J. Mol. Sci. 2019, 20(2), 272; https://doi.org/10.3390/ijms20020272

Brain-Derived Neurotrophin and TrkB in Head and Neck Squamous Cell Carcinoma

Department of Otorhinolaryngology, Medical University of Innsbruck, Anichstrasse 35, A-6020 Innsbruck, Austria
*
Author to whom correspondence should be addressed.
Received: 30 November 2018 / Revised: 3 January 2019 / Accepted: 5 January 2019 / Published: 11 January 2019
(This article belongs to the Special Issue Brain-Derived Neurotrophic Factor 2018)
Full-Text   |   PDF [3479 KB, uploaded 11 January 2019]   |  
  |   Review Reports

Abstract

We hypothesized that in head and neck squamous cell carcinoma (HNSCC), the neurotrophin brain-derived neurotrophic factor (BDNF) and its high affinity receptor TrkB regulate tumor cell survival, invasion, and therapy resistance. We used in situ hybridization for BDNF and immunohistochemistry (IHC) for TrkB in 131 HNSCC samples. Brain-derived neurotrophic factor was highly expressed in normal mucosa in HNSCC tissue and in cell lines, whereas only 42.74% of HNSCC tissue was TrkB+. One fourth of HNSCC cases was human papilloma virus (HPV) positive, but the TrkB IHC frequency was not different in HPV-positive (HPV+) and negative cases. The UPCI-SCC090 cells expressed constitutive levels of TrkB. Transforming-growth-factor-β1 (1 ng/mL TGF-β1) induced TrkB in a subpopulation of SCC-25 cells. A single 10-µg/mL mitomycin C treatment in UPCI-SCC090 cells induced apoptosis and BDNF did not rescue them. The SCC-25 cells were resistant to the MMC treatment, and their growth decreased after TGF-β1 treatment, but was restored by BDNF if it followed TGF-β1. Taken together, BDNF might be ineffective in HPV+ HNSCC patients. In HPV HNSCC patients, tumor cells did not die after chemotherapeutic challenge and BDNF with TGF-β1 could improve tumor cell survival and contribute to worse patient prognosis. View Full-Text
Keywords: epithelial–mesenchymal transition; vimentin; cytokeratin; p53 mutation; paraffin embedding; riboprobe epithelial–mesenchymal transition; vimentin; cytokeratin; p53 mutation; paraffin embedding; riboprobe
Figures

Graphical abstract

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 (CC BY 4.0).

Supplementary material

SciFeed

Share & Cite This Article

MDPI and ACS Style

Dudás, J.; Riml, A.; Tuertscher, R.; Pritz, C.; Steinbichler, T.B.; Schartinger, V.H.; Sprung, S.; Glueckert, R.; Schrott-Fischer, A.; Johnson Chacko, L.; Riechelmann, H. Brain-Derived Neurotrophin and TrkB in Head and Neck Squamous Cell Carcinoma. Int. J. Mol. Sci. 2019, 20, 272.

Show more citation formats Show less citations formats

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

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top