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STK33 overexpression in hypopharyngeal squamous cell carcinoma: possible role in tumorigenesis
BACKGROUND: The role of serine/threonine kinase 33 (STK33) gene in tumorigenesis is still controversial. This study was aimed to investigate whether STK33 had the effect on hypopharyngeal squamous cell carcinoma (HSCC) and relevant genes, as well as the potential relation to ERK1/2 pathway. METHODS:...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4305229/ https://www.ncbi.nlm.nih.gov/pubmed/25603720 http://dx.doi.org/10.1186/s12885-015-1009-3 |
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author | Huang, Lingyan Chen, Chen Zhang, Guodong Ju, Yuanrong Zhang, Jianzhong Wang, Haibo Li, Jianfeng |
author_facet | Huang, Lingyan Chen, Chen Zhang, Guodong Ju, Yuanrong Zhang, Jianzhong Wang, Haibo Li, Jianfeng |
author_sort | Huang, Lingyan |
collection | PubMed |
description | BACKGROUND: The role of serine/threonine kinase 33 (STK33) gene in tumorigenesis is still controversial. This study was aimed to investigate whether STK33 had the effect on hypopharyngeal squamous cell carcinoma (HSCC) and relevant genes, as well as the potential relation to ERK1/2 pathway. METHODS: Immunohistochemistry was performed to investigate STK33 expression in human HSCC specimens. MTT, immunofluorescence, clone formation and matrigel invasion assays were employed to detect the effects of STK33 knockdown (STK33-RNAi) and/or PD98059 on major oncogenic properties of a HSCC cell line (Fadu), while, real-time PCR and western blot were used to examine the expressions of relevant genes. RESULTS: STK33 was over-expressed in HSCC specimens, which was significantly associated with certain clinicopathological parameters. STK33-RNAi in Fadu cells resulted in inhibition of proliferation, induction of apoptosis, reduction of clone formation, and decline in the migration and invasion. These effects were potentiated by administration of PD98059. Mechanistic studies revealed that STK33-RNAi led to an increase in Caspse-3, Nm-23-H1 and E-Cadherin expressions and a reduction in Bcl-2, Ki-67 and Vimentin expressions. Moreover, PD98059 significantly reduced both ERK1/2 and STK33 expressions in Fadu cells. CONCLUSIONS: STK33 is a potential oncogene and a promising diagnostic marker for HSCC. STK33 may promote tumorigenesis and progression of HSCC, and serve as a valuable molecular target for treatment of HSCC. |
format | Online Article Text |
id | pubmed-4305229 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-43052292015-02-03 STK33 overexpression in hypopharyngeal squamous cell carcinoma: possible role in tumorigenesis Huang, Lingyan Chen, Chen Zhang, Guodong Ju, Yuanrong Zhang, Jianzhong Wang, Haibo Li, Jianfeng BMC Cancer Research Article BACKGROUND: The role of serine/threonine kinase 33 (STK33) gene in tumorigenesis is still controversial. This study was aimed to investigate whether STK33 had the effect on hypopharyngeal squamous cell carcinoma (HSCC) and relevant genes, as well as the potential relation to ERK1/2 pathway. METHODS: Immunohistochemistry was performed to investigate STK33 expression in human HSCC specimens. MTT, immunofluorescence, clone formation and matrigel invasion assays were employed to detect the effects of STK33 knockdown (STK33-RNAi) and/or PD98059 on major oncogenic properties of a HSCC cell line (Fadu), while, real-time PCR and western blot were used to examine the expressions of relevant genes. RESULTS: STK33 was over-expressed in HSCC specimens, which was significantly associated with certain clinicopathological parameters. STK33-RNAi in Fadu cells resulted in inhibition of proliferation, induction of apoptosis, reduction of clone formation, and decline in the migration and invasion. These effects were potentiated by administration of PD98059. Mechanistic studies revealed that STK33-RNAi led to an increase in Caspse-3, Nm-23-H1 and E-Cadherin expressions and a reduction in Bcl-2, Ki-67 and Vimentin expressions. Moreover, PD98059 significantly reduced both ERK1/2 and STK33 expressions in Fadu cells. CONCLUSIONS: STK33 is a potential oncogene and a promising diagnostic marker for HSCC. STK33 may promote tumorigenesis and progression of HSCC, and serve as a valuable molecular target for treatment of HSCC. BioMed Central 2015-01-21 /pmc/articles/PMC4305229/ /pubmed/25603720 http://dx.doi.org/10.1186/s12885-015-1009-3 Text en © Huang et al.; licensee BioMed Central. 2015 This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Article Huang, Lingyan Chen, Chen Zhang, Guodong Ju, Yuanrong Zhang, Jianzhong Wang, Haibo Li, Jianfeng STK33 overexpression in hypopharyngeal squamous cell carcinoma: possible role in tumorigenesis |
title | STK33 overexpression in hypopharyngeal squamous cell carcinoma: possible role in tumorigenesis |
title_full | STK33 overexpression in hypopharyngeal squamous cell carcinoma: possible role in tumorigenesis |
title_fullStr | STK33 overexpression in hypopharyngeal squamous cell carcinoma: possible role in tumorigenesis |
title_full_unstemmed | STK33 overexpression in hypopharyngeal squamous cell carcinoma: possible role in tumorigenesis |
title_short | STK33 overexpression in hypopharyngeal squamous cell carcinoma: possible role in tumorigenesis |
title_sort | stk33 overexpression in hypopharyngeal squamous cell carcinoma: possible role in tumorigenesis |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4305229/ https://www.ncbi.nlm.nih.gov/pubmed/25603720 http://dx.doi.org/10.1186/s12885-015-1009-3 |
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