Ethyl p-methoxycinnamate inhibits tumor growth by suppressing of fatty acid synthesis and depleting ATP
Abstract Cancer cells reprogram their energy metabolism pathways, but the mechanisms that enable them to meet their energy demands remain poorly understood. This study investigates the anticancer effects of ethyl p-methoxycinnamate (EMC) in Ehrlich ascites tumor cells (EATCs) and reveals that de nov...
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Nature Portfolio
2025-05-01
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| Series: | Scientific Reports |
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| Online Access: | https://doi.org/10.1038/s41598-025-00131-1 |
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| author | Yutaro Sasaki Niina Mizushima Toshio Norikura Isao Matsui-Yuasa Akiko Kojima-Yuasa |
| author_facet | Yutaro Sasaki Niina Mizushima Toshio Norikura Isao Matsui-Yuasa Akiko Kojima-Yuasa |
| author_sort | Yutaro Sasaki |
| collection | DOAJ |
| description | Abstract Cancer cells reprogram their energy metabolism pathways, but the mechanisms that enable them to meet their energy demands remain poorly understood. This study investigates the anticancer effects of ethyl p-methoxycinnamate (EMC) in Ehrlich ascites tumor cells (EATCs) and reveals that de novo fatty acid synthesis, rather than glycolysis, plays a pivotal role in sustaining energy homeostasis in cancer cells. EMC significantly reduced ATP levels despite enhancing glycolytic activity. It suppressed the expression of key enzymes involved in de novo fatty acid synthesis, including Acly, Acc1, and Fasn, resulting in decreased intracellular triglyceride (TG) levels. The addition of exogenous palmitic acid reversed EMC-induced ATP depletion and mitigated its anti-proliferative effects. Mechanistically, the ATP reduction caused by EMC was associated with inhibition of the c-Myc/SREBP1 pathway and arrest of the G1/S cell cycle transition. These findings demonstrate that EMC inhibits EATC proliferation by reducing ATP levels via suppression of de novo fatty acid synthesis. This study highlights the critical role of de novo fatty acid synthesis, rather than glycolysis, in maintaining energy homeostasis in cancer cells and provides novel insights into targeting cancer metabolism. |
| format | Article |
| id | doaj-art-0d33e4365e564e369ca9bc898d8c2c3a |
| institution | OA Journals |
| issn | 2045-2322 |
| language | English |
| publishDate | 2025-05-01 |
| publisher | Nature Portfolio |
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| series | Scientific Reports |
| spelling | doaj-art-0d33e4365e564e369ca9bc898d8c2c3a2025-08-20T02:10:50ZengNature PortfolioScientific Reports2045-23222025-05-0115111510.1038/s41598-025-00131-1Ethyl p-methoxycinnamate inhibits tumor growth by suppressing of fatty acid synthesis and depleting ATPYutaro Sasaki0Niina Mizushima1Toshio Norikura2Isao Matsui-Yuasa3Akiko Kojima-Yuasa4Department of Nutrition, Graduate School of Human Life and Ecology, Osaka Metropolitan UniversityDepartment of Nutrition, Graduate School of Human Life and Ecology, Osaka Metropolitan UniversityDepartment of Nutrition, Aomori University of Health and WelfareDepartment of Nutrition, Graduate School of Human Life and Ecology, Osaka Metropolitan UniversityDepartment of Nutrition, Graduate School of Human Life and Ecology, Osaka Metropolitan UniversityAbstract Cancer cells reprogram their energy metabolism pathways, but the mechanisms that enable them to meet their energy demands remain poorly understood. This study investigates the anticancer effects of ethyl p-methoxycinnamate (EMC) in Ehrlich ascites tumor cells (EATCs) and reveals that de novo fatty acid synthesis, rather than glycolysis, plays a pivotal role in sustaining energy homeostasis in cancer cells. EMC significantly reduced ATP levels despite enhancing glycolytic activity. It suppressed the expression of key enzymes involved in de novo fatty acid synthesis, including Acly, Acc1, and Fasn, resulting in decreased intracellular triglyceride (TG) levels. The addition of exogenous palmitic acid reversed EMC-induced ATP depletion and mitigated its anti-proliferative effects. Mechanistically, the ATP reduction caused by EMC was associated with inhibition of the c-Myc/SREBP1 pathway and arrest of the G1/S cell cycle transition. These findings demonstrate that EMC inhibits EATC proliferation by reducing ATP levels via suppression of de novo fatty acid synthesis. This study highlights the critical role of de novo fatty acid synthesis, rather than glycolysis, in maintaining energy homeostasis in cancer cells and provides novel insights into targeting cancer metabolism.https://doi.org/10.1038/s41598-025-00131-1Kaempferia galanga L.Ethyl p-methoxycinnamateDe Novo fatty acid synthesisGlycolysisATPEhrlich Ascites tumor cells |
| spellingShingle | Yutaro Sasaki Niina Mizushima Toshio Norikura Isao Matsui-Yuasa Akiko Kojima-Yuasa Ethyl p-methoxycinnamate inhibits tumor growth by suppressing of fatty acid synthesis and depleting ATP Scientific Reports Kaempferia galanga L. Ethyl p-methoxycinnamate De Novo fatty acid synthesis Glycolysis ATP Ehrlich Ascites tumor cells |
| title | Ethyl p-methoxycinnamate inhibits tumor growth by suppressing of fatty acid synthesis and depleting ATP |
| title_full | Ethyl p-methoxycinnamate inhibits tumor growth by suppressing of fatty acid synthesis and depleting ATP |
| title_fullStr | Ethyl p-methoxycinnamate inhibits tumor growth by suppressing of fatty acid synthesis and depleting ATP |
| title_full_unstemmed | Ethyl p-methoxycinnamate inhibits tumor growth by suppressing of fatty acid synthesis and depleting ATP |
| title_short | Ethyl p-methoxycinnamate inhibits tumor growth by suppressing of fatty acid synthesis and depleting ATP |
| title_sort | ethyl p methoxycinnamate inhibits tumor growth by suppressing of fatty acid synthesis and depleting atp |
| topic | Kaempferia galanga L. Ethyl p-methoxycinnamate De Novo fatty acid synthesis Glycolysis ATP Ehrlich Ascites tumor cells |
| url | https://doi.org/10.1038/s41598-025-00131-1 |
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