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Effects of selective cyclooxygenase‐2 inhibitor robenacoxib on primary cells derived from feline injection‐site sarcoma
Feline injection‐site sarcomas (FISSs) are highly invasive malignant mesenchymal neoplasms that arise from injection sites in cats. Although the tumorigenesis of FISSs is still uncertain, there is a consensus that FISS is associated with chronic inflammation caused by irritation of injection‐related...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10399534/ https://www.ncbi.nlm.nih.gov/pubmed/37334757 http://dx.doi.org/10.1111/jcmm.17717 |
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author | Lu, Chen‐Hui Yu, Shu‐Han Wu, Ching‐Ho Yeh, Jason Lih‐Seng Chang, Hui‐Wen Jeng, Chian‐Ren Chang, Yen‐Chen |
author_facet | Lu, Chen‐Hui Yu, Shu‐Han Wu, Ching‐Ho Yeh, Jason Lih‐Seng Chang, Hui‐Wen Jeng, Chian‐Ren Chang, Yen‐Chen |
author_sort | Lu, Chen‐Hui |
collection | PubMed |
description | Feline injection‐site sarcomas (FISSs) are highly invasive malignant mesenchymal neoplasms that arise from injection sites in cats. Although the tumorigenesis of FISSs is still uncertain, there is a consensus that FISS is associated with chronic inflammation caused by irritation of injection‐related trauma and foreign chemical substances. Chronic inflammation can provide a proper microenvironment for tumour development, which has been known as one of the risk factors of tumorigenesis in many tumours. To investigate the tumorigenesis of FISS and screen for its potential therapeutic targets, cyclooxygenase‐2 (COX‐2), an inflammation‐enhancing enzyme, was selected as a target for this study. In vitro experiments using FISS‐ and normal tissue‐derived primary cells and robenacoxib, a highly selective COX‐2 inhibitor, were performed. The results demonstrated that expression of COX‐2 could be detected in formalin‐fixed and paraffin‐embedded FISS tissues and FISS‐derived primary cells. Cell viability, migration and colony formation of FISS‐derived primary cells were inhibited, and cell apoptosis was enhanced by robenacoxib in a dose‐dependent manner. However, susceptibility to robenacoxib varied in different lines of FISS primary cells and was not completely correlated with COX‐2 expression. Our results suggest that COX‐2 inhibitors could be potential adjuvant therapeutics against FISSs. |
format | Online Article Text |
id | pubmed-10399534 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-103995342023-08-04 Effects of selective cyclooxygenase‐2 inhibitor robenacoxib on primary cells derived from feline injection‐site sarcoma Lu, Chen‐Hui Yu, Shu‐Han Wu, Ching‐Ho Yeh, Jason Lih‐Seng Chang, Hui‐Wen Jeng, Chian‐Ren Chang, Yen‐Chen J Cell Mol Med Original Articles Feline injection‐site sarcomas (FISSs) are highly invasive malignant mesenchymal neoplasms that arise from injection sites in cats. Although the tumorigenesis of FISSs is still uncertain, there is a consensus that FISS is associated with chronic inflammation caused by irritation of injection‐related trauma and foreign chemical substances. Chronic inflammation can provide a proper microenvironment for tumour development, which has been known as one of the risk factors of tumorigenesis in many tumours. To investigate the tumorigenesis of FISS and screen for its potential therapeutic targets, cyclooxygenase‐2 (COX‐2), an inflammation‐enhancing enzyme, was selected as a target for this study. In vitro experiments using FISS‐ and normal tissue‐derived primary cells and robenacoxib, a highly selective COX‐2 inhibitor, were performed. The results demonstrated that expression of COX‐2 could be detected in formalin‐fixed and paraffin‐embedded FISS tissues and FISS‐derived primary cells. Cell viability, migration and colony formation of FISS‐derived primary cells were inhibited, and cell apoptosis was enhanced by robenacoxib in a dose‐dependent manner. However, susceptibility to robenacoxib varied in different lines of FISS primary cells and was not completely correlated with COX‐2 expression. Our results suggest that COX‐2 inhibitors could be potential adjuvant therapeutics against FISSs. John Wiley and Sons Inc. 2023-06-19 /pmc/articles/PMC10399534/ /pubmed/37334757 http://dx.doi.org/10.1111/jcmm.17717 Text en © 2023 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Lu, Chen‐Hui Yu, Shu‐Han Wu, Ching‐Ho Yeh, Jason Lih‐Seng Chang, Hui‐Wen Jeng, Chian‐Ren Chang, Yen‐Chen Effects of selective cyclooxygenase‐2 inhibitor robenacoxib on primary cells derived from feline injection‐site sarcoma |
title | Effects of selective cyclooxygenase‐2 inhibitor robenacoxib on primary cells derived from feline injection‐site sarcoma |
title_full | Effects of selective cyclooxygenase‐2 inhibitor robenacoxib on primary cells derived from feline injection‐site sarcoma |
title_fullStr | Effects of selective cyclooxygenase‐2 inhibitor robenacoxib on primary cells derived from feline injection‐site sarcoma |
title_full_unstemmed | Effects of selective cyclooxygenase‐2 inhibitor robenacoxib on primary cells derived from feline injection‐site sarcoma |
title_short | Effects of selective cyclooxygenase‐2 inhibitor robenacoxib on primary cells derived from feline injection‐site sarcoma |
title_sort | effects of selective cyclooxygenase‐2 inhibitor robenacoxib on primary cells derived from feline injection‐site sarcoma |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10399534/ https://www.ncbi.nlm.nih.gov/pubmed/37334757 http://dx.doi.org/10.1111/jcmm.17717 |
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