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Hispolon induces apoptosis in oral squamous cell carcinoma cells through JNK/HO‐1 pathway activation

Oral squamous cell carcinoma (OSCC) has a high recurrence rate and poor prognosis. Hispolon, a polyphenolic compound with antiviral, antioxidant, and anticancer activities, is a potential chemotherapy agent. However, few studies have investigated the anti‐cancer mechanism of hispolon in oral cancer....

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Autores principales: Yang, Wei‐En, Chen, Yi‐Tzu, Su, Chun‐Wen, Chen, Mu‐Kuan, Yeh, Chia‐Ming, Chen, Yen‐Lin, Tsai, Meng‐Ying, Yang, Shun‐Fa, Lin, Chiao‐Wen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10148051/
https://www.ncbi.nlm.nih.gov/pubmed/36967712
http://dx.doi.org/10.1111/jcmm.17729
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author Yang, Wei‐En
Chen, Yi‐Tzu
Su, Chun‐Wen
Chen, Mu‐Kuan
Yeh, Chia‐Ming
Chen, Yen‐Lin
Tsai, Meng‐Ying
Yang, Shun‐Fa
Lin, Chiao‐Wen
author_facet Yang, Wei‐En
Chen, Yi‐Tzu
Su, Chun‐Wen
Chen, Mu‐Kuan
Yeh, Chia‐Ming
Chen, Yen‐Lin
Tsai, Meng‐Ying
Yang, Shun‐Fa
Lin, Chiao‐Wen
author_sort Yang, Wei‐En
collection PubMed
description Oral squamous cell carcinoma (OSCC) has a high recurrence rate and poor prognosis. Hispolon, a polyphenolic compound with antiviral, antioxidant, and anticancer activities, is a potential chemotherapy agent. However, few studies have investigated the anti‐cancer mechanism of hispolon in oral cancer. This present study used the cell viability assay, clonogenic assay, fluorescent nuclear staining, and flow cytometry assay to analyse the apoptosis‐inducing effects of hispolon in OSCC cells. After hispolon treatment, the apoptotic initiators, cleaved caspase‐3, −8, and − 9, were upregulated, whereas the cellular inhibitor of apoptosis protein‐1 (cIAP1) was downregulated. Furthermore, a proteome profile analysis using a human apoptosis array revealed the overexpression of heme oxygenase‐1 (HO‐1) by hispolon, which was determined to be involved in caspase‐dependent apoptosis. Moreover, cotreatment with hispolon and mitogen‐activated protein kinase (MAPK) inhibitors revealed that hispolon induces apoptosis in OSCC cells through activation of the c‐Jun N‐terminal kinase (JNK) pathway and not the extracellular signal‐regulated kinase (ERK) or p38 pathway. These findings indicate that hispolon may exert an anticancer effect on oral cancer cells by upregulating HO‐1 and inducing caspase‐dependent apoptosis by activating the JNK pathway.
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spelling pubmed-101480512023-04-30 Hispolon induces apoptosis in oral squamous cell carcinoma cells through JNK/HO‐1 pathway activation Yang, Wei‐En Chen, Yi‐Tzu Su, Chun‐Wen Chen, Mu‐Kuan Yeh, Chia‐Ming Chen, Yen‐Lin Tsai, Meng‐Ying Yang, Shun‐Fa Lin, Chiao‐Wen J Cell Mol Med Original Articles Oral squamous cell carcinoma (OSCC) has a high recurrence rate and poor prognosis. Hispolon, a polyphenolic compound with antiviral, antioxidant, and anticancer activities, is a potential chemotherapy agent. However, few studies have investigated the anti‐cancer mechanism of hispolon in oral cancer. This present study used the cell viability assay, clonogenic assay, fluorescent nuclear staining, and flow cytometry assay to analyse the apoptosis‐inducing effects of hispolon in OSCC cells. After hispolon treatment, the apoptotic initiators, cleaved caspase‐3, −8, and − 9, were upregulated, whereas the cellular inhibitor of apoptosis protein‐1 (cIAP1) was downregulated. Furthermore, a proteome profile analysis using a human apoptosis array revealed the overexpression of heme oxygenase‐1 (HO‐1) by hispolon, which was determined to be involved in caspase‐dependent apoptosis. Moreover, cotreatment with hispolon and mitogen‐activated protein kinase (MAPK) inhibitors revealed that hispolon induces apoptosis in OSCC cells through activation of the c‐Jun N‐terminal kinase (JNK) pathway and not the extracellular signal‐regulated kinase (ERK) or p38 pathway. These findings indicate that hispolon may exert an anticancer effect on oral cancer cells by upregulating HO‐1 and inducing caspase‐dependent apoptosis by activating the JNK pathway. John Wiley and Sons Inc. 2023-03-27 /pmc/articles/PMC10148051/ /pubmed/36967712 http://dx.doi.org/10.1111/jcmm.17729 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
Yang, Wei‐En
Chen, Yi‐Tzu
Su, Chun‐Wen
Chen, Mu‐Kuan
Yeh, Chia‐Ming
Chen, Yen‐Lin
Tsai, Meng‐Ying
Yang, Shun‐Fa
Lin, Chiao‐Wen
Hispolon induces apoptosis in oral squamous cell carcinoma cells through JNK/HO‐1 pathway activation
title Hispolon induces apoptosis in oral squamous cell carcinoma cells through JNK/HO‐1 pathway activation
title_full Hispolon induces apoptosis in oral squamous cell carcinoma cells through JNK/HO‐1 pathway activation
title_fullStr Hispolon induces apoptosis in oral squamous cell carcinoma cells through JNK/HO‐1 pathway activation
title_full_unstemmed Hispolon induces apoptosis in oral squamous cell carcinoma cells through JNK/HO‐1 pathway activation
title_short Hispolon induces apoptosis in oral squamous cell carcinoma cells through JNK/HO‐1 pathway activation
title_sort hispolon induces apoptosis in oral squamous cell carcinoma cells through jnk/ho‐1 pathway activation
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10148051/
https://www.ncbi.nlm.nih.gov/pubmed/36967712
http://dx.doi.org/10.1111/jcmm.17729
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