Yan-Jia Du, Jin-Peng Lv, Yao Fu, Meng Lan, Jing-Feng Li, Hui Zhang, Nan Wu
{"title":"Dauriporphine通过miR-424-5p/MAPK14轴抑制肺癌细胞活力、运动性和能量代谢。","authors":"Yan-Jia Du, Jin-Peng Lv, Yao Fu, Meng Lan, Jing-Feng Li, Hui Zhang, Nan Wu","doi":"10.1186/s41065-025-00473-w","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Dauriporphine is a major ingredient of Manispernum daericum DC., which has been demonstrated to show wide anti-tumor activities. miR-424-5p, as a regulator of lung cancer, was hypothesized to serve as the therapeutic target for dauriporphine This study evaluated the potential of dauriporphine in treating lung adenocarcinoma and revealed the underlying molecular mechanism.</p><p><strong>Results: </strong>The anti-tumor effect of dauriporphine on lung adenocarcinoma was assessed in A549 cells, and it was found that dauriporphine significantly inhibited the viability of A549 cells in a concentration-dependent manner with the half maximal inhibitory concentration (IC<sub>50</sub>) value of 10.57 µM. Dauriporphine induced decreasing cell growth, motility, and energy metabolism, indicating the anti-tumor effect of dauriporphine on A549 cells. Dauriporphine inducing elevated miR-424-5p levels, while silencing miR-424-5p significantly recovered cell viability, migration, and energy metabolism of A549 cells. Mitogen-activated protein Kinase 14 (MAPK14) was negatively regulated by miR-424-5p, and the knockdown of MAPK14 could reverse the protective effect of miR-424-5p on dauriporphine-treated A549 cells.</p><p><strong>Conclusion: </strong>Dauriporphine inhibited cell growth, metastasis, and glycolysis-related energy metabolism of lung adenocarcinoma cells via modulating miR-424-5p/MAPK14 axis. Dauriporphine can be considered in drug development for lung adenocarcinoma.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"101"},"PeriodicalIF":2.5000,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12153179/pdf/","citationCount":"0","resultStr":"{\"title\":\"Dauriporphine inhibited lung cancer cell viability, motility, and energy metabolism through the miR-424-5p/MAPK14 axis.\",\"authors\":\"Yan-Jia Du, Jin-Peng Lv, Yao Fu, Meng Lan, Jing-Feng Li, Hui Zhang, Nan Wu\",\"doi\":\"10.1186/s41065-025-00473-w\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Dauriporphine is a major ingredient of Manispernum daericum DC., which has been demonstrated to show wide anti-tumor activities. miR-424-5p, as a regulator of lung cancer, was hypothesized to serve as the therapeutic target for dauriporphine This study evaluated the potential of dauriporphine in treating lung adenocarcinoma and revealed the underlying molecular mechanism.</p><p><strong>Results: </strong>The anti-tumor effect of dauriporphine on lung adenocarcinoma was assessed in A549 cells, and it was found that dauriporphine significantly inhibited the viability of A549 cells in a concentration-dependent manner with the half maximal inhibitory concentration (IC<sub>50</sub>) value of 10.57 µM. Dauriporphine induced decreasing cell growth, motility, and energy metabolism, indicating the anti-tumor effect of dauriporphine on A549 cells. Dauriporphine inducing elevated miR-424-5p levels, while silencing miR-424-5p significantly recovered cell viability, migration, and energy metabolism of A549 cells. Mitogen-activated protein Kinase 14 (MAPK14) was negatively regulated by miR-424-5p, and the knockdown of MAPK14 could reverse the protective effect of miR-424-5p on dauriporphine-treated A549 cells.</p><p><strong>Conclusion: </strong>Dauriporphine inhibited cell growth, metastasis, and glycolysis-related energy metabolism of lung adenocarcinoma cells via modulating miR-424-5p/MAPK14 axis. Dauriporphine can be considered in drug development for lung adenocarcinoma.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>\",\"PeriodicalId\":12862,\"journal\":{\"name\":\"Hereditas\",\"volume\":\"162 1\",\"pages\":\"101\"},\"PeriodicalIF\":2.5000,\"publicationDate\":\"2025-06-11\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12153179/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Hereditas\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1186/s41065-025-00473-w\",\"RegionNum\":3,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Hereditas","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1186/s41065-025-00473-w","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Dauriporphine inhibited lung cancer cell viability, motility, and energy metabolism through the miR-424-5p/MAPK14 axis.
Background: Dauriporphine is a major ingredient of Manispernum daericum DC., which has been demonstrated to show wide anti-tumor activities. miR-424-5p, as a regulator of lung cancer, was hypothesized to serve as the therapeutic target for dauriporphine This study evaluated the potential of dauriporphine in treating lung adenocarcinoma and revealed the underlying molecular mechanism.
Results: The anti-tumor effect of dauriporphine on lung adenocarcinoma was assessed in A549 cells, and it was found that dauriporphine significantly inhibited the viability of A549 cells in a concentration-dependent manner with the half maximal inhibitory concentration (IC50) value of 10.57 µM. Dauriporphine induced decreasing cell growth, motility, and energy metabolism, indicating the anti-tumor effect of dauriporphine on A549 cells. Dauriporphine inducing elevated miR-424-5p levels, while silencing miR-424-5p significantly recovered cell viability, migration, and energy metabolism of A549 cells. Mitogen-activated protein Kinase 14 (MAPK14) was negatively regulated by miR-424-5p, and the knockdown of MAPK14 could reverse the protective effect of miR-424-5p on dauriporphine-treated A549 cells.
Conclusion: Dauriporphine inhibited cell growth, metastasis, and glycolysis-related energy metabolism of lung adenocarcinoma cells via modulating miR-424-5p/MAPK14 axis. Dauriporphine can be considered in drug development for lung adenocarcinoma.
HereditasBiochemistry, Genetics and Molecular Biology-Genetics
CiteScore
3.80
自引率
3.70%
发文量
0
期刊介绍:
For almost a century, Hereditas has published original cutting-edge research and reviews. As the Official journal of the Mendelian Society of Lund, the journal welcomes research from across all areas of genetics and genomics. Topics of interest include human and medical genetics, animal and plant genetics, microbial genetics, agriculture and bioinformatics.