Nerve Growth Factor (NGF)-Receptor Survival Axis in Head and Neck Squamous Cell Carcinoma
Neurotrophins and their receptors might regulate cell survival in head and neck squamous cell carcinoma (HNSCC). mRNA expression of nerve growth factor (NGF) and protein synthesis of high (NTRK1) and low affinity neurotrophin (p75 neurotrophin receptor; NTR) receptors were investigated in normal ora...
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| Veröffentlicht in: | International journal of molecular sciences 2018-06, Vol.19 (6), p.1771 |
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| creator | Dudás, József Dietl, Wolfgang Romani, Angela Reinold, Susanne Glueckert, Rudolf Schrott-Fischer, Anneliese Dejaco, Daniel Johnson Chacko, Lejo Tuertscher, Raphaela Schartinger, Volker Hans Riechelmann, Herbert |
| description | Neurotrophins and their receptors might regulate cell survival in head and neck squamous cell carcinoma (HNSCC). mRNA expression of nerve growth factor (NGF) and protein synthesis of high (NTRK1) and low affinity neurotrophin (p75 neurotrophin receptor; NTR) receptors were investigated in normal oral mucosa and in HNSCC. HNSCC cell lines were treated with mitomycin C (MMC) and cell survival was investigated. Normal and malignant epithelial cells expressed NGF mRNA. NTRK1 was upregulated in 80% of HNSCC tissue, and 50% of HNSCC samples were p75NTR positive. Interestingly, in HNSCC tissue: NTRK1 and p75NTR immunohistochemical reactions were mutually exclusive. Detroit 562 cell line contained only p75NTR, UPCI-SCC090 cells synthesized NTRK1 but not p75NTR and SCC-25 culture had p75NTR and NTRK1 in different cells. NGF (100 ng/mL) significantly improved (1.4-fold) the survival of cultured UPCI-SCC090 cells after MMC-induced cell cycle arrest, while Detroit 562 cells with high levels of p75NTR did not even get arrested by single short MMC treatment. p75NTR in HNSCC might be related with NGF-independent therapy resistance, while NTRK1 might transduce a survival signal of NGF and contribute in this way to improved tumor cell survival after cell cycle arrest. |
| doi_str_mv | 10.3390/ijms19061771 |
| format | Article |
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HNSCC cell lines were treated with mitomycin C (MMC) and cell survival was investigated. Normal and malignant epithelial cells expressed NGF mRNA. NTRK1 was upregulated in 80% of HNSCC tissue, and 50% of HNSCC samples were p75NTR positive. Interestingly, in HNSCC tissue: NTRK1 and p75NTR immunohistochemical reactions were mutually exclusive. Detroit 562 cell line contained only p75NTR, UPCI-SCC090 cells synthesized NTRK1 but not p75NTR and SCC-25 culture had p75NTR and NTRK1 in different cells. NGF (100 ng/mL) significantly improved (1.4-fold) the survival of cultured UPCI-SCC090 cells after MMC-induced cell cycle arrest, while Detroit 562 cells with high levels of p75NTR did not even get arrested by single short MMC treatment. p75NTR in HNSCC might be related with NGF-independent therapy resistance, while NTRK1 might transduce a survival signal of NGF and contribute in this way to improved tumor cell survival after cell cycle arrest.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms19061771</identifier><identifier>PMID: 29904026</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Biomarkers, Tumor - genetics ; Biomarkers, Tumor - metabolism ; Carcinoma, Squamous Cell - metabolism ; Carcinoma, Squamous Cell - pathology ; Cell culture ; Cell Cycle ; Cell Line, Tumor ; Cell Survival ; Epithelial cells ; Gene expression ; Growth factors ; Head & neck cancer ; Head and Neck Neoplasms - genetics ; Head and Neck Neoplasms - metabolism ; Head and Neck Neoplasms - pathology ; Humans ; Mitomycin C ; Mouth Mucosa - metabolism ; Mouth Mucosa - pathology ; Mucosa ; Nerve growth factor ; Nerve Growth Factor - genetics ; Nerve Growth Factor - metabolism ; Nerve Tissue Proteins - genetics ; Nerve Tissue Proteins - metabolism ; Neurotrophic factors ; Protein biosynthesis ; Protein synthesis ; Proteins ; Receptor, trkA - genetics ; Receptor, trkA - metabolism ; Receptors, Nerve Growth Factor - genetics ; Receptors, Nerve Growth Factor - metabolism ; Squamous cell carcinoma ; Survival</subject><ispartof>International journal of molecular sciences, 2018-06, Vol.19 (6), p.1771</ispartof><rights>2018. This work is licensed under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2018 by the authors. 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c478t-265483f1e9b50ce26864aabb3e0ae649746d9f9481e69e2cc93ea386ae1caefb3</citedby><cites>FETCH-LOGICAL-c478t-265483f1e9b50ce26864aabb3e0ae649746d9f9481e69e2cc93ea386ae1caefb3</cites><orcidid>0000-0002-2528-1449 ; 0000-0002-9877-3399</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6032238/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6032238/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,883,27911,27912,53778,53780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29904026$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dudás, József</creatorcontrib><creatorcontrib>Dietl, Wolfgang</creatorcontrib><creatorcontrib>Romani, Angela</creatorcontrib><creatorcontrib>Reinold, Susanne</creatorcontrib><creatorcontrib>Glueckert, Rudolf</creatorcontrib><creatorcontrib>Schrott-Fischer, Anneliese</creatorcontrib><creatorcontrib>Dejaco, Daniel</creatorcontrib><creatorcontrib>Johnson Chacko, Lejo</creatorcontrib><creatorcontrib>Tuertscher, Raphaela</creatorcontrib><creatorcontrib>Schartinger, Volker Hans</creatorcontrib><creatorcontrib>Riechelmann, Herbert</creatorcontrib><title>Nerve Growth Factor (NGF)-Receptor Survival Axis in Head and Neck Squamous Cell Carcinoma</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Neurotrophins and their receptors might regulate cell survival in head and neck squamous cell carcinoma (HNSCC). mRNA expression of nerve growth factor (NGF) and protein synthesis of high (NTRK1) and low affinity neurotrophin (p75 neurotrophin receptor; NTR) receptors were investigated in normal oral mucosa and in HNSCC. HNSCC cell lines were treated with mitomycin C (MMC) and cell survival was investigated. Normal and malignant epithelial cells expressed NGF mRNA. NTRK1 was upregulated in 80% of HNSCC tissue, and 50% of HNSCC samples were p75NTR positive. Interestingly, in HNSCC tissue: NTRK1 and p75NTR immunohistochemical reactions were mutually exclusive. Detroit 562 cell line contained only p75NTR, UPCI-SCC090 cells synthesized NTRK1 but not p75NTR and SCC-25 culture had p75NTR and NTRK1 in different cells. NGF (100 ng/mL) significantly improved (1.4-fold) the survival of cultured UPCI-SCC090 cells after MMC-induced cell cycle arrest, while Detroit 562 cells with high levels of p75NTR did not even get arrested by single short MMC treatment. p75NTR in HNSCC might be related with NGF-independent therapy resistance, while NTRK1 might transduce a survival signal of NGF and contribute in this way to improved tumor cell survival after cell cycle arrest.</description><subject>Biomarkers, Tumor - genetics</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Carcinoma, Squamous Cell - metabolism</subject><subject>Carcinoma, Squamous Cell - pathology</subject><subject>Cell culture</subject><subject>Cell Cycle</subject><subject>Cell Line, Tumor</subject><subject>Cell Survival</subject><subject>Epithelial cells</subject><subject>Gene expression</subject><subject>Growth factors</subject><subject>Head & neck cancer</subject><subject>Head and Neck Neoplasms - genetics</subject><subject>Head and Neck Neoplasms - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dudás, József</au><au>Dietl, Wolfgang</au><au>Romani, Angela</au><au>Reinold, Susanne</au><au>Glueckert, Rudolf</au><au>Schrott-Fischer, Anneliese</au><au>Dejaco, Daniel</au><au>Johnson Chacko, Lejo</au><au>Tuertscher, Raphaela</au><au>Schartinger, Volker Hans</au><au>Riechelmann, Herbert</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nerve Growth Factor (NGF)-Receptor Survival Axis in Head and Neck Squamous Cell Carcinoma</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2018-06-14</date><risdate>2018</risdate><volume>19</volume><issue>6</issue><spage>1771</spage><pages>1771-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>Neurotrophins and their receptors might regulate cell survival in head and neck squamous cell carcinoma (HNSCC). mRNA expression of nerve growth factor (NGF) and protein synthesis of high (NTRK1) and low affinity neurotrophin (p75 neurotrophin receptor; NTR) receptors were investigated in normal oral mucosa and in HNSCC. HNSCC cell lines were treated with mitomycin C (MMC) and cell survival was investigated. Normal and malignant epithelial cells expressed NGF mRNA. NTRK1 was upregulated in 80% of HNSCC tissue, and 50% of HNSCC samples were p75NTR positive. Interestingly, in HNSCC tissue: NTRK1 and p75NTR immunohistochemical reactions were mutually exclusive. Detroit 562 cell line contained only p75NTR, UPCI-SCC090 cells synthesized NTRK1 but not p75NTR and SCC-25 culture had p75NTR and NTRK1 in different cells. NGF (100 ng/mL) significantly improved (1.4-fold) the survival of cultured UPCI-SCC090 cells after MMC-induced cell cycle arrest, while Detroit 562 cells with high levels of p75NTR did not even get arrested by single short MMC treatment. p75NTR in HNSCC might be related with NGF-independent therapy resistance, while NTRK1 might transduce a survival signal of NGF and contribute in this way to improved tumor cell survival after cell cycle arrest.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>29904026</pmid><doi>10.3390/ijms19061771</doi><orcidid>https://orcid.org/0000-0002-2528-1449</orcidid><orcidid>https://orcid.org/0000-0002-9877-3399</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Biomarkers, Tumor - genetics Biomarkers, Tumor - metabolism Carcinoma, Squamous Cell - metabolism Carcinoma, Squamous Cell - pathology Cell culture Cell Cycle Cell Line, Tumor Cell Survival Epithelial cells Gene expression Growth factors Head & neck cancer Head and Neck Neoplasms - genetics Head and Neck Neoplasms - metabolism Head and Neck Neoplasms - pathology Humans Mitomycin C Mouth Mucosa - metabolism Mouth Mucosa - pathology Mucosa Nerve growth factor Nerve Growth Factor - genetics Nerve Growth Factor - metabolism Nerve Tissue Proteins - genetics Nerve Tissue Proteins - metabolism Neurotrophic factors Protein biosynthesis Protein synthesis Proteins Receptor, trkA - genetics Receptor, trkA - metabolism Receptors, Nerve Growth Factor - genetics Receptors, Nerve Growth Factor - metabolism Squamous cell carcinoma Survival |
| title | Nerve Growth Factor (NGF)-Receptor Survival Axis in Head and Neck Squamous Cell Carcinoma |
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