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HSP90AA1 promotes lymphatic metastasis of hypopharyngeal squamous cell carcinoma by regulating epithelial-mesenchymal transition
BACKGROUND: Lymphatic metastasis (LM) emerges as an independent prognostic marker for hypopharyngeal squamous cell carcinoma (HSPSCC), chiefly contributing to treatment inefficacy. This study aimed to scrutinize the prognostic relevance of HSP90AA1 and its potential regulatory mechanism of concernin...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Tech Science Press
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10398399/ https://www.ncbi.nlm.nih.gov/pubmed/37547757 http://dx.doi.org/10.32604/or.2023.030081 |
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author | TANG, FENGXIANG LI, YANSHI PAN, MIN WANG, ZHIHAI LU, TAO LIU, CHUAN ZHOU, XIN HU, GUOHUA |
author_facet | TANG, FENGXIANG LI, YANSHI PAN, MIN WANG, ZHIHAI LU, TAO LIU, CHUAN ZHOU, XIN HU, GUOHUA |
author_sort | TANG, FENGXIANG |
collection | PubMed |
description | BACKGROUND: Lymphatic metastasis (LM) emerges as an independent prognostic marker for hypopharyngeal squamous cell carcinoma (HSPSCC), chiefly contributing to treatment inefficacy. This study aimed to scrutinize the prognostic relevance of HSP90AA1 and its potential regulatory mechanism of concerning LM in HPSCC. METHODS: In a preceding investigation, HSP90AA1, a differential gene, was discovered through transcriptome sequencing of HPSCC tissues, considering both the presence and absence of LM. Validation of HSP90AA1 expression was accomplished via qRT-PCR, western-blotting(WB), and immunohistochemistry(IHC), while its prognostic significance was assessed employing Kaplan–Meier survival analysis(KMSA), log-rank test(LR), and Cox’s regression analysis(CRA). Bioinformatics techniques facilitated the prediction and analysis of its plausible mechanisms in LM, further substantiated by in vitro and in vivo experiments utilizing FaDu cell lines. RESULTS: HSP90AA1 is substantially up-regulated in HPSCC with LM and is identified as an independent prognostic risk determinant. The down-regulation of HSP90AA1 can achieve inhibition of tumor cell proliferation, migration and invasion. Both in vivo experiments and Bioinformatics exploration hint at promoting LM by Epithelial-mesenchymal transition (EMT), regulated by HSP90AA1. CONCLUSIONS: HSP90AA1, by controlling EMT, can foster LM in HPSCC.This finding sets the foundation for delving into new therapeutic targets for HPSCC. |
format | Online Article Text |
id | pubmed-10398399 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Tech Science Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-103983992023-08-04 HSP90AA1 promotes lymphatic metastasis of hypopharyngeal squamous cell carcinoma by regulating epithelial-mesenchymal transition TANG, FENGXIANG LI, YANSHI PAN, MIN WANG, ZHIHAI LU, TAO LIU, CHUAN ZHOU, XIN HU, GUOHUA Oncol Res Article BACKGROUND: Lymphatic metastasis (LM) emerges as an independent prognostic marker for hypopharyngeal squamous cell carcinoma (HSPSCC), chiefly contributing to treatment inefficacy. This study aimed to scrutinize the prognostic relevance of HSP90AA1 and its potential regulatory mechanism of concerning LM in HPSCC. METHODS: In a preceding investigation, HSP90AA1, a differential gene, was discovered through transcriptome sequencing of HPSCC tissues, considering both the presence and absence of LM. Validation of HSP90AA1 expression was accomplished via qRT-PCR, western-blotting(WB), and immunohistochemistry(IHC), while its prognostic significance was assessed employing Kaplan–Meier survival analysis(KMSA), log-rank test(LR), and Cox’s regression analysis(CRA). Bioinformatics techniques facilitated the prediction and analysis of its plausible mechanisms in LM, further substantiated by in vitro and in vivo experiments utilizing FaDu cell lines. RESULTS: HSP90AA1 is substantially up-regulated in HPSCC with LM and is identified as an independent prognostic risk determinant. The down-regulation of HSP90AA1 can achieve inhibition of tumor cell proliferation, migration and invasion. Both in vivo experiments and Bioinformatics exploration hint at promoting LM by Epithelial-mesenchymal transition (EMT), regulated by HSP90AA1. CONCLUSIONS: HSP90AA1, by controlling EMT, can foster LM in HPSCC.This finding sets the foundation for delving into new therapeutic targets for HPSCC. Tech Science Press 2023-07-21 /pmc/articles/PMC10398399/ /pubmed/37547757 http://dx.doi.org/10.32604/or.2023.030081 Text en © 2023 Tang et al. https://creativecommons.org/licenses/by/4.0/This work is licensed under a Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Article TANG, FENGXIANG LI, YANSHI PAN, MIN WANG, ZHIHAI LU, TAO LIU, CHUAN ZHOU, XIN HU, GUOHUA HSP90AA1 promotes lymphatic metastasis of hypopharyngeal squamous cell carcinoma by regulating epithelial-mesenchymal transition |
title | HSP90AA1 promotes lymphatic metastasis of hypopharyngeal squamous cell carcinoma by regulating epithelial-mesenchymal transition |
title_full | HSP90AA1 promotes lymphatic metastasis of hypopharyngeal squamous cell carcinoma by regulating epithelial-mesenchymal transition |
title_fullStr | HSP90AA1 promotes lymphatic metastasis of hypopharyngeal squamous cell carcinoma by regulating epithelial-mesenchymal transition |
title_full_unstemmed | HSP90AA1 promotes lymphatic metastasis of hypopharyngeal squamous cell carcinoma by regulating epithelial-mesenchymal transition |
title_short | HSP90AA1 promotes lymphatic metastasis of hypopharyngeal squamous cell carcinoma by regulating epithelial-mesenchymal transition |
title_sort | hsp90aa1 promotes lymphatic metastasis of hypopharyngeal squamous cell carcinoma by regulating epithelial-mesenchymal transition |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10398399/ https://www.ncbi.nlm.nih.gov/pubmed/37547757 http://dx.doi.org/10.32604/or.2023.030081 |
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