Epoxymicheliolide Reduces Radiation‐Induced Senescence and Extracellular Matrix Formation by Disrupting NF‐κB and TGF‐β/SMAD Pathways in Lung Cancer
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| Format: | Artículo Open Access |
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Wiley
2024
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| _version_ | 1867016284155150336 |
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| author | Heng Zhou Yong Chen Ningzu Jiang Yanxian Ren Jiayuan Zhuang Yue Ren Lin Shen Chenghao Li |
| author_facet | Heng Zhou Yong Chen Ningzu Jiang Yanxian Ren Jiayuan Zhuang Yue Ren Lin Shen Chenghao Li Heng Zhou Yong Chen Ningzu Jiang Yanxian Ren Jiayuan Zhuang Yue Ren Lin Shen Chenghao Li |
| collection | Wiley Open Access |
| contents | Epoxymicheliolide Reduces Radiation‐Induced Senescence and Extracellular Matrix Formation by Disrupting NF‐κB and TGF‐β/SMAD Pathways in Lung Cancer Heng Zhou Yong Chen Ningzu Jiang Yanxian Ren Jiayuan Zhuang Yue Ren Lin Shen Chenghao Li Phytotherapy Research ABSTRACTLung cancer is a major cause of cancer‐related mortality, and radiotherapy is often limited by tumor resistance and side effects. This study explores whether epoxymicheliolide (ECL), a compound from feverfew, can enhance radiotherapy efficacy in lung cancer. We tested ECL on A549 and PC‐9 lung cancer cell lines to evaluate its effect on x‐ray irradiation. We measured apoptosis, NF‐κB pathway inhibition, TGF‐β secretion reduction, and epithelial‐mesenchymal transition suppression. In vivo, C57BL/6 mice with lung tumors received ECL and radiotherapy. ECL enhanced the antiproliferative effects of x‐ray irradiation, induced apoptosis in senescent cells, inhibited the NF‐κB pathway, reduced TGF‐β levels, and suppressed epithelial‐mesenchymal transition. ECL also inhibited tumor growth and improved survival in mice. ECL is a promising adjunct to radiotherapy for lung cancer, improving treatment outcomes by targeting multiple tumor progression mechanisms. It offers potential for enhanced management of lung cancer. 10.1002/ptr.8352 http://onlinelibrary.wiley.com/termsAndConditions#vor |
| doi_str_mv | 10.1002/ptr.8352 |
| format | Artículo Open Access |
| id | wiley_oa_10_1002_ptr_8352 |
| institution | Wiley Open Access |
| license_str_mv | http://onlinelibrary.wiley.com/termsAndConditions#vor |
| publishDate | 2024 |
| publisher | Wiley |
| record_format | wiley_oa |
| spellingShingle | Epoxymicheliolide Reduces Radiation‐Induced Senescence and Extracellular Matrix Formation by Disrupting NF‐κB and TGF‐β/SMAD Pathways in Lung Cancer Heng Zhou Yong Chen Ningzu Jiang Yanxian Ren Jiayuan Zhuang Yue Ren Lin Shen Chenghao Li Phytotherapy Research Epoxymicheliolide Reduces Radiation‐Induced Senescence and Extracellular Matrix Formation by Disrupting NF‐κB and TGF‐β/SMAD Pathways in Lung Cancer Heng Zhou Yong Chen Ningzu Jiang Yanxian Ren Jiayuan Zhuang Yue Ren Lin Shen Chenghao Li Phytotherapy Research ABSTRACTLung cancer is a major cause of cancer‐related mortality, and radiotherapy is often limited by tumor resistance and side effects. This study explores whether epoxymicheliolide (ECL), a compound from feverfew, can enhance radiotherapy efficacy in lung cancer. We tested ECL on A549 and PC‐9 lung cancer cell lines to evaluate its effect on x‐ray irradiation. We measured apoptosis, NF‐κB pathway inhibition, TGF‐β secretion reduction, and epithelial‐mesenchymal transition suppression. In vivo, C57BL/6 mice with lung tumors received ECL and radiotherapy. ECL enhanced the antiproliferative effects of x‐ray irradiation, induced apoptosis in senescent cells, inhibited the NF‐κB pathway, reduced TGF‐β levels, and suppressed epithelial‐mesenchymal transition. ECL also inhibited tumor growth and improved survival in mice. ECL is a promising adjunct to radiotherapy for lung cancer, improving treatment outcomes by targeting multiple tumor progression mechanisms. It offers potential for enhanced management of lung cancer. 10.1002/ptr.8352 http://onlinelibrary.wiley.com/termsAndConditions#vor |
| title | Epoxymicheliolide Reduces Radiation‐Induced Senescence and Extracellular Matrix Formation by Disrupting NF‐κB and TGF‐β/SMAD Pathways in Lung Cancer |
| topic | Phytotherapy Research |
| url | https://onlinelibrary.wiley.com/doi/10.1002/ptr.8352 |