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7,8-Dihydroxyflavone induces mitochondrial apoptosis and down-regulates the expression of ganglioside GD3 in malignant melanoma cells
Malignant melanoma is a skin cancer with poor prognosis and high resistance to conventional treatment. 7,8-dihydroxyflavone (7,8-DHF) has shown anti-carcinogenic, anti-inflammatory, anti-oxidant, and pharmacological effects in several types of cancer. However, the relationship between ganglioside ex...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Springer US
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10060447/ https://www.ncbi.nlm.nih.gov/pubmed/36991237 http://dx.doi.org/10.1007/s12672-023-00643-0 |
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author | Ju, Won Seok Seo, Sang Young Mun, Seong-eun Kim, Kyongtae Yu, Jin Ok Ryu, Jae-Sung Kim, Ji-Su Choo, Young-Kug |
author_facet | Ju, Won Seok Seo, Sang Young Mun, Seong-eun Kim, Kyongtae Yu, Jin Ok Ryu, Jae-Sung Kim, Ji-Su Choo, Young-Kug |
author_sort | Ju, Won Seok |
collection | PubMed |
description | Malignant melanoma is a skin cancer with poor prognosis and high resistance to conventional treatment. 7,8-dihydroxyflavone (7,8-DHF) has shown anti-carcinogenic, anti-inflammatory, anti-oxidant, and pharmacological effects in several types of cancer. However, the relationship between ganglioside expression and the anti-cancer effects of 7,8-DHF in melanoma is not fully understood. In the present study, 7,8-DHF exhibits specific anti-proliferation, anti-migration, and G2/M phase cell-cycle arrest effects on both melanoma cancer cell lines, and induces mitochondrial dysfunction and apoptosis, making it a potent candidate for anti-melanoma treatment. Furthermore, we confirmed that 7,8-DHF significantly reduces the expression levels of ganglioside GD3 and its synthase, which are known to be closely involved in carcinogenesis. Taken together, our findings suggest that 7,8-DHF may be a potent anti-cancer drug candidate for the treatment of malignant melanoma. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12672-023-00643-0. |
format | Online Article Text |
id | pubmed-10060447 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Springer US |
record_format | MEDLINE/PubMed |
spelling | pubmed-100604472023-03-31 7,8-Dihydroxyflavone induces mitochondrial apoptosis and down-regulates the expression of ganglioside GD3 in malignant melanoma cells Ju, Won Seok Seo, Sang Young Mun, Seong-eun Kim, Kyongtae Yu, Jin Ok Ryu, Jae-Sung Kim, Ji-Su Choo, Young-Kug Discov Oncol Research Malignant melanoma is a skin cancer with poor prognosis and high resistance to conventional treatment. 7,8-dihydroxyflavone (7,8-DHF) has shown anti-carcinogenic, anti-inflammatory, anti-oxidant, and pharmacological effects in several types of cancer. However, the relationship between ganglioside expression and the anti-cancer effects of 7,8-DHF in melanoma is not fully understood. In the present study, 7,8-DHF exhibits specific anti-proliferation, anti-migration, and G2/M phase cell-cycle arrest effects on both melanoma cancer cell lines, and induces mitochondrial dysfunction and apoptosis, making it a potent candidate for anti-melanoma treatment. Furthermore, we confirmed that 7,8-DHF significantly reduces the expression levels of ganglioside GD3 and its synthase, which are known to be closely involved in carcinogenesis. Taken together, our findings suggest that 7,8-DHF may be a potent anti-cancer drug candidate for the treatment of malignant melanoma. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12672-023-00643-0. Springer US 2023-03-30 /pmc/articles/PMC10060447/ /pubmed/36991237 http://dx.doi.org/10.1007/s12672-023-00643-0 Text en © The Author(s) 2023, corrected publication 2023 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 Ju, Won Seok Seo, Sang Young Mun, Seong-eun Kim, Kyongtae Yu, Jin Ok Ryu, Jae-Sung Kim, Ji-Su Choo, Young-Kug 7,8-Dihydroxyflavone induces mitochondrial apoptosis and down-regulates the expression of ganglioside GD3 in malignant melanoma cells |
title | 7,8-Dihydroxyflavone induces mitochondrial apoptosis and down-regulates the expression of ganglioside GD3 in malignant melanoma cells |
title_full | 7,8-Dihydroxyflavone induces mitochondrial apoptosis and down-regulates the expression of ganglioside GD3 in malignant melanoma cells |
title_fullStr | 7,8-Dihydroxyflavone induces mitochondrial apoptosis and down-regulates the expression of ganglioside GD3 in malignant melanoma cells |
title_full_unstemmed | 7,8-Dihydroxyflavone induces mitochondrial apoptosis and down-regulates the expression of ganglioside GD3 in malignant melanoma cells |
title_short | 7,8-Dihydroxyflavone induces mitochondrial apoptosis and down-regulates the expression of ganglioside GD3 in malignant melanoma cells |
title_sort | 7,8-dihydroxyflavone induces mitochondrial apoptosis and down-regulates the expression of ganglioside gd3 in malignant melanoma cells |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10060447/ https://www.ncbi.nlm.nih.gov/pubmed/36991237 http://dx.doi.org/10.1007/s12672-023-00643-0 |
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