Isoliquiritigenin induces HMOX1 and GPX4-mediated ferroptosis in gallbladder cancer cells
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Le résumé fourni par la source
BACKGROUND: Gallbladder cancer (GBC) is the most common malignant tumor of biliary tract. Isoliquiritigenin (ISL) is a natural compound with chalcone structure extracted from the roots of licorice and other plants. Relevant studies have shown that ISL has a strong anti-tumor ability in various types of tumors. However, the research of ISL against GBC has not been reported, which needs to be further investigated. METHODS: The effects of ISL against GBC cells in vitro and in vivo were characterized by cytotoxicity test, RNA-sequencing, quantitative real-time polymerase chain reaction, reactive oxygen species (ROS) detection, lipid peroxidation detection, ferrous ion detection, glutathione disulphide/glutathione (GSSG/GSH) detection, lentivirus transfection, nude mice tumorigenesis experiment and immunohistochemistry. RESULTS: ISL significantly inhibited the proliferation of GBC cells in vitro . The results of transcriptome sequencing and bioinformatics analysis showed that ferroptosis was the main pathway of ISL inhibiting the proliferation of GBC, and HMOX1 and GPX4 were the key molecules of ISL-induced ferroptosis. Knockdown of HMOX1 or overexpression of GPX4 can reduce the sensitivity of GBC cells to ISL-induced ferroptosis and significantly restore the viability of GBC cells. Moreover, ISL significantly reversed the iron content, ROS level, lipid peroxidation level and GSSG/GSH ratio of GBC cells. Finally, ISL significantly inhibited the growth of GBC in vivo and regulated the ferroptosis of GBC by mediating HMOX1 and GPX4 . CONCLUSION: ISL induced ferroptosis in GBC mainly by activating p62-Keap1-Nrf2-HMOX1 signaling pathway and down-regulating GPX4 in vitro and in vivo . This evidence may provide a new direction for the treatment of GBC.
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Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- Isoliquiritigenin induces HMOX1 and GPX4-mediated ferroptosis in gallbladder cancer cells
- Date Crossref
- 24/07/2023
- Éditeur
- Ovid Technologies (Wolters Kluwer Health)
- Type
- journal-article
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.
Où se fait cette recherche
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Shanghai Jiao Tong University Department of Biliary-Pancreatic Surgery pays non établi dans la noticeUniversité ou école supérieure
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Renji Hospital pays non établi dans la noticeÉtablissement de santé
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Shanghai Cancer Institute pays non établi dans la noticeStructure de recherche
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State Key Laboratory of Oncogene and Related Genes pays non établi dans la noticeStructure de recherche
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Shanghai Chest Hospital pays non établi dans la noticeÉtablissement de santé
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XinHua Hospital pays non établi dans la noticeÉtablissement de santé
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University of Shanghai for Science and Technology pays non établi dans la noticeUniversité ou école supérieure
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Nanjing University of Chinese Medicine Department of General Surgery pays non établi dans la noticeUniversité ou école supérieure
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Shanghai Research Center of Biliary Tract Disease pays non établi dans la noticeStructure de recherche
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School of Medicine State Key Laboratory of Oncogenes and Related Genes pays non établi dans la noticeUniversité ou école supérieure
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How to cite this article: Wang ZY pays non établi dans la noticeInstitution
Department of Biliary-Pancreatic Surgery — Shanghai Jiao Tong University, Renji Hospital et Shanghai Cancer Institute, avec 8 autres affiliations.
Une affiliation ne permet pas de déduire la nationalité d’un auteur.