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CD155 promotes radioresistance and malignancy of esophageal cancer by regulating Hippo-YAP pathway
The expression of CD155 has been observed to increase in various human cancers, but its role in the development of esophageal cancer (EC) is unclear. Radiotherapy is one of the primary therapeutic options for EC. However, radioresistance is still a severe issue in EC treatment. In this study, Oncomi...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer US
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9243211/ https://www.ncbi.nlm.nih.gov/pubmed/35768666 http://dx.doi.org/10.1007/s12672-022-00515-z |
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author | Xin, Huixian Liu, Yuchen Chen, Pengxiang Yin, Tianwen Wang, Meijie Liu, Tianyu Wen, Zhihua Cheng, Yufeng |
author_facet | Xin, Huixian Liu, Yuchen Chen, Pengxiang Yin, Tianwen Wang, Meijie Liu, Tianyu Wen, Zhihua Cheng, Yufeng |
author_sort | Xin, Huixian |
collection | PubMed |
description | The expression of CD155 has been observed to increase in various human cancers, but its role in the development of esophageal cancer (EC) is unclear. Radiotherapy is one of the primary therapeutic options for EC. However, radioresistance is still a severe issue in EC treatment. In this study, Oncomine database mining, immunohistochemistry, and survival analysis showed that higher expression of CD155 in patients with EC than in healthy controls. In vitro and in vivo, we found for the first time that irradiation increased the expression of CD155 in EC cells. CD155 knockdown inhibited cell proliferation and migration and tumor formation, and significantly increased radiosensitivity in EC. The in vivo model with high CD155 expression significantly promoted the proliferation and migration of EC cells. Furthermore, increased CD155 expression was associated with poor prognosis in patients with EC. CD155 regulated the Hippo-Yap pathway, influencing cell proliferation and migration. Therefore, CD155 is essential for the proliferation, migration, and radioresistance of EC. CD155 inhibition may be a viable strategy for improving radiation treatment efficacy in individuals with EC. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12672-022-00515-z. |
format | Online Article Text |
id | pubmed-9243211 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Springer US |
record_format | MEDLINE/PubMed |
spelling | pubmed-92432112022-07-01 CD155 promotes radioresistance and malignancy of esophageal cancer by regulating Hippo-YAP pathway Xin, Huixian Liu, Yuchen Chen, Pengxiang Yin, Tianwen Wang, Meijie Liu, Tianyu Wen, Zhihua Cheng, Yufeng Discov Oncol Research The expression of CD155 has been observed to increase in various human cancers, but its role in the development of esophageal cancer (EC) is unclear. Radiotherapy is one of the primary therapeutic options for EC. However, radioresistance is still a severe issue in EC treatment. In this study, Oncomine database mining, immunohistochemistry, and survival analysis showed that higher expression of CD155 in patients with EC than in healthy controls. In vitro and in vivo, we found for the first time that irradiation increased the expression of CD155 in EC cells. CD155 knockdown inhibited cell proliferation and migration and tumor formation, and significantly increased radiosensitivity in EC. The in vivo model with high CD155 expression significantly promoted the proliferation and migration of EC cells. Furthermore, increased CD155 expression was associated with poor prognosis in patients with EC. CD155 regulated the Hippo-Yap pathway, influencing cell proliferation and migration. Therefore, CD155 is essential for the proliferation, migration, and radioresistance of EC. CD155 inhibition may be a viable strategy for improving radiation treatment efficacy in individuals with EC. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12672-022-00515-z. Springer US 2022-06-29 /pmc/articles/PMC9243211/ /pubmed/35768666 http://dx.doi.org/10.1007/s12672-022-00515-z Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Research Xin, Huixian Liu, Yuchen Chen, Pengxiang Yin, Tianwen Wang, Meijie Liu, Tianyu Wen, Zhihua Cheng, Yufeng CD155 promotes radioresistance and malignancy of esophageal cancer by regulating Hippo-YAP pathway |
title | CD155 promotes radioresistance and malignancy of esophageal cancer by regulating Hippo-YAP pathway |
title_full | CD155 promotes radioresistance and malignancy of esophageal cancer by regulating Hippo-YAP pathway |
title_fullStr | CD155 promotes radioresistance and malignancy of esophageal cancer by regulating Hippo-YAP pathway |
title_full_unstemmed | CD155 promotes radioresistance and malignancy of esophageal cancer by regulating Hippo-YAP pathway |
title_short | CD155 promotes radioresistance and malignancy of esophageal cancer by regulating Hippo-YAP pathway |
title_sort | cd155 promotes radioresistance and malignancy of esophageal cancer by regulating hippo-yap pathway |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9243211/ https://www.ncbi.nlm.nih.gov/pubmed/35768666 http://dx.doi.org/10.1007/s12672-022-00515-z |
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