Didymin Inhibits Proliferation and Induces Apoptosis in Gastric Cancer Cells by Modulating the PI3K/Akt Pathway.
Gastric cancer (GC) is a malignant tumor with high morbidity and mortality rates worldwide. This study aimed to investigate the effects and mechanisms of action of didymin, a dietary flavonoid glycoside, on GC treatment. Human GC cell lines Hs-746T and AGS were used to assess the effects of didymin...
| Publicado en: | Nutrition & Cancer Vol. 77; no. 4/5; pp. 537 - 553 |
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| Autores principales: | , |
| Formato: | pictorial research tables/charts Journal Article |
| Publicado: |
Taylor & Francis Ltd
2025
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| Acceso en línea: | Ver este registro en EBSCOhost |
| fields | @attributes: recordID: 1 pdfLink: plink: https://search.ebscohost.com/login.aspx?direct=true&db=ccm&AN=184162668&site=ehost-live header: @attributes: shortDbName: ccm uiTerm: 184162668 longDbName: CINAHL Complete uiTag: AN controlInfo: bkinfo: dissinfo: jinfo: jid: 01635581 7MS jtl: Nutrition & Cancer issn: 01635581 maglogo: N pubinfo: dt: 2025 vid: 77 iid: 4/5 pid: 377 pub: Taylor & Francis Ltd place: Philadelphia, Pennsylvania artinfo: ui: 184162668 182384660 184162668 184162668 10.1080/01635581.2025.2454050 184162668 ppf: 537 ppct: 16 formats: fmt: – @attributes: type: T – @attributes: type: P tig: atl: Didymin Inhibits Proliferation and Induces Apoptosis in Gastric Cancer Cells by Modulating the PI3K/Akt Pathway. aug: au: Zhang, Tong Xu, Bin affil: Department of General Surgery, General Hospital of Northern Theater Command, Shenyang, China sug: subj: Stomach Neoplasms Drug Therapy Flavonoids Antagonists and Inhibitors Flavonoids Pharmacodynamics Flavonoids Therapeutic Use Glycosides Therapeutic Use Dietary Supplementation Cell Proliferation Drug Effects Apoptosis Drug Effects Signal Transduction Drug Efficacy Animal Studies Mice In Vivo Studies In Vitro Studies Cell Line, Tumor Cell Viability Cell Cycle Wound Healing Reactive Oxygen Species Mitochondria Xenografts Phosphorylation ab: Gastric cancer (GC) is a malignant tumor with high morbidity and mortality rates worldwide. This study aimed to investigate the effects and mechanisms of action of didymin, a dietary flavonoid glycoside, on GC treatment. Human GC cell lines Hs-746T and AGS were used to assess the effects of didymin on cell viability, cell proliferation, and cell cycle. The results showed that didymin decreased the proliferative capacity of GC cells and blocked cell cycle. Didymin decreased wound healing, invasion, and migration capacities of GC cells. Mitochondrial reactive oxygen species (ROS) levels and mitochondrial membrane potentials were reduced in cells treated with didymin. Network pharmacology analysis revealed that the therapeutic effects of didymin on AGS cells were related to the phosphatidylinositol 3-kinase (PI3K)/Akt pathway. In vivo mouse xenograft studies confirmed that didymin treatment decreased tumor cell proliferation, cell cycle protein levels, and Akt phosphorylation. The present study demonstrated that didymin regulates mitochondrial function and the PI3K/Akt pathway to inhibit cell proliferation and induce apoptosis in GC cells in vitro and in vivo. Therefore, didymin is a promising drug for the treatment of GC. pubtype: Academic Journal doctype: pictorial research tables/charts Journal Article ougenre: Article language: English refInfo: holdings: @attributes: islocal: N |
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