Paeonol represses A549 cell glycolytic reprogramming and proliferation by decreasing m6A modification of Acyl-CoA dehydrogenase
Aberrant glycolytic reprogramming is involved in lung cancer progression by promoting the proliferation of non-small cell lung cancer cells. Paeonol, as a traditional Chinese medicine, plays a critical role in multiple cancer cell proliferation and inflammation. Acyl-CoA dehydrogenase (ACADM) is inv...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
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Wolters Kluwer Medknow Publications
2023-01-01
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| Series: | Chinese Journal of Physiology |
| Subjects: | |
| Online Access: | http://www.cjphysiology.org/article.asp?issn=0304-4920;year=2023;volume=66;issue=4;spage=248;epage=256;aulast=Zhang |
| _version_ | 1827783387114373120 |
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| author | Lixin Zhang Lihua Wu Xiangrui Zhu Jian Mei Yingli Chen |
| author_facet | Lixin Zhang Lihua Wu Xiangrui Zhu Jian Mei Yingli Chen |
| author_sort | Lixin Zhang |
| collection | DOAJ |
| description | Aberrant glycolytic reprogramming is involved in lung cancer progression by promoting the proliferation of non-small cell lung cancer cells. Paeonol, as a traditional Chinese medicine, plays a critical role in multiple cancer cell proliferation and inflammation. Acyl-CoA dehydrogenase (ACADM) is involved in the development of metabolic diseases. N6-methyladenosine (m6A) modification is important for the regulation of messenger RNA stability, splicing, and translation. Here, we investigated whether paeonol regulates the proliferation and glycolytic reprogramming via ACADM with m6A modification in A549 cells (human non-small cell lung cancer cells). Cell counting kit 8, 5-Bromo-2-deoxyuridine, 5-ethynyl-2'-deoxyuridine (EdU) incorporation, flow cytometry analysis, western blotting and seahorse XFe24 extracellular flux analyzer assays showed that paeonol had a significant inhibitory effect against A549 cell proliferation and glycolysis. Mechanistically, ACADM was a functional target of paeonol. We also showed that the m6A reader YTH domain containing 1 plays an important role in m6A-modified ACADM expression, which is negatively regulated by paeonol, and is involved in A549 cell proliferation and glycolytic reprogramming. These results indicated the central function of paeonol in regulating A549 cell glycolytic reprogramming and proliferation via m6A modification of ACADM. |
| first_indexed | 2024-03-11T15:46:54Z |
| format | Article |
| id | doaj.art-3bbdd9434be64d16bd2e80c42fb22bf9 |
| institution | Directory Open Access Journal |
| issn | 0304-4920 2666-0059 |
| language | English |
| last_indexed | 2024-03-11T15:46:54Z |
| publishDate | 2023-01-01 |
| publisher | Wolters Kluwer Medknow Publications |
| record_format | Article |
| series | Chinese Journal of Physiology |
| spelling | doaj.art-3bbdd9434be64d16bd2e80c42fb22bf92023-10-26T06:13:23ZengWolters Kluwer Medknow PublicationsChinese Journal of Physiology0304-49202666-00592023-01-0166424825610.4103/cjop.CJOP-D-22-00166Paeonol represses A549 cell glycolytic reprogramming and proliferation by decreasing m6A modification of Acyl-CoA dehydrogenaseLixin ZhangLihua WuXiangrui ZhuJian MeiYingli ChenAberrant glycolytic reprogramming is involved in lung cancer progression by promoting the proliferation of non-small cell lung cancer cells. Paeonol, as a traditional Chinese medicine, plays a critical role in multiple cancer cell proliferation and inflammation. Acyl-CoA dehydrogenase (ACADM) is involved in the development of metabolic diseases. N6-methyladenosine (m6A) modification is important for the regulation of messenger RNA stability, splicing, and translation. Here, we investigated whether paeonol regulates the proliferation and glycolytic reprogramming via ACADM with m6A modification in A549 cells (human non-small cell lung cancer cells). Cell counting kit 8, 5-Bromo-2-deoxyuridine, 5-ethynyl-2'-deoxyuridine (EdU) incorporation, flow cytometry analysis, western blotting and seahorse XFe24 extracellular flux analyzer assays showed that paeonol had a significant inhibitory effect against A549 cell proliferation and glycolysis. Mechanistically, ACADM was a functional target of paeonol. We also showed that the m6A reader YTH domain containing 1 plays an important role in m6A-modified ACADM expression, which is negatively regulated by paeonol, and is involved in A549 cell proliferation and glycolytic reprogramming. These results indicated the central function of paeonol in regulating A549 cell glycolytic reprogramming and proliferation via m6A modification of ACADM.http://www.cjphysiology.org/article.asp?issn=0304-4920;year=2023;volume=66;issue=4;spage=248;epage=256;aulast=Zhangacyl-coa dehydrogenaseglycolytic reprogrammingn6-methyladenosinepaeonolproliferation |
| spellingShingle | Lixin Zhang Lihua Wu Xiangrui Zhu Jian Mei Yingli Chen Paeonol represses A549 cell glycolytic reprogramming and proliferation by decreasing m6A modification of Acyl-CoA dehydrogenase Chinese Journal of Physiology acyl-coa dehydrogenase glycolytic reprogramming n6-methyladenosine paeonol proliferation |
| title | Paeonol represses A549 cell glycolytic reprogramming and proliferation by decreasing m6A modification of Acyl-CoA dehydrogenase |
| title_full | Paeonol represses A549 cell glycolytic reprogramming and proliferation by decreasing m6A modification of Acyl-CoA dehydrogenase |
| title_fullStr | Paeonol represses A549 cell glycolytic reprogramming and proliferation by decreasing m6A modification of Acyl-CoA dehydrogenase |
| title_full_unstemmed | Paeonol represses A549 cell glycolytic reprogramming and proliferation by decreasing m6A modification of Acyl-CoA dehydrogenase |
| title_short | Paeonol represses A549 cell glycolytic reprogramming and proliferation by decreasing m6A modification of Acyl-CoA dehydrogenase |
| title_sort | paeonol represses a549 cell glycolytic reprogramming and proliferation by decreasing m6a modification of acyl coa dehydrogenase |
| topic | acyl-coa dehydrogenase glycolytic reprogramming n6-methyladenosine paeonol proliferation |
| url | http://www.cjphysiology.org/article.asp?issn=0304-4920;year=2023;volume=66;issue=4;spage=248;epage=256;aulast=Zhang |
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