S'abonner

Dendrobium nobile active ingredient Dendrobin A against hepatocellular carcinoma via inhibiting nuclear factor kappa-B signaling - 23/07/24

Doi : 10.1016/j.biopha.2024.117013 
Yaping Yu a, 1, Yonghao Fan a, 1, Wenli Mei b, 1, Xiaoqing Xu a, Yan Chen a, Yangyang Zhao a, Banzhan Ruan a, Zhihua Shen c, Yanda Lu a, , Shaojiang Zheng a, , Wei Jie a,
a Key Laboratory of Emergency and Trauma of Ministry of Education, Engineering Research Center for Hainan Biological Sample Resources of Major Diseases & the Department of Oncology of the First Affiliated Hospital, Hainan Medical University, Haikou 570102, PR China 
b Key Laboratory of Natural Products Research and Development from Li Folk Medicine of Hainan Province, Institute of Tropical Bioscience and Biotechnology, Chinese Academy of Tropical Agricultural Sciences, Haikou 571199, PR China 
c Department of Pathophysiology, School of Basic Medicine Sciences, Guangdong Medical University, Zhanjiang 524023, PR China 

Corresponding authors.

Abstract

Objective

Dendrobin A, a typical active ingredient of the traditional Chinese medicine Dendrobium nobile, has potential clinical application in cancer treatment; however, its effect and mechanism in anti-hepatocellular carcinoma (HCC) remain unsolved.

Method

The effects of Dendrobin A on the viability, migration, invasion, cycle, apoptosis, and epithelial-mesenchymal transition of HepG2 and SK-HEP-1 cells were verified by in vitro experiments. mRNA sequencing was performed to screen the differentially expressed genes (DEGs) of HCC cells before and after Dendrobin A treatment, following GO enrichment and KEGG signaling pathway analyses. Mechanistically, molecular docking was used to evaluate the binding of Dendrobin A with proteins p65 and p50, before further verifying the activation of nuclear factor kappa-B (NF-κB) signaling. Finally, the antiproliferative effect of Dendrobin A on HCC cells was explored through animal experiments.

Results

Dendrobin A arrested cell cycle, induced apoptosis, and inhibited proliferation, migration, invasion, and blocked epithelial-mesenchymal transition in HepG2 and SK-HEP-1 cells. mRNA sequencing identified 830 DEGs, involving various biological processes. KEGG analysis highlighted NF-κB signaling. Molecular docking revealed strong binding of Dendrobin A with p65 and p50 proteins, and western blotting confirmed reduced levels of p-p65 and p-p50 in HCC cells post Dendrobin A treatment. NF-κB agonist PMA reversed Dendrobin A-inhibited cell proliferation migration and invasion. In vivo experiments showed that Dendrobin A inhibited HCC cell growth.

Conclusion

Our findings suggest that Dendrobin A exhibits anti-HCC properties by inhibiting the activation of the NF-κB pathway. These results provide a scientific basis for utilizing Dendrobium nobile in anti-HCC therapies.

Le texte complet de cet article est disponible en PDF.

Graphical Abstract




 : 

The active compound Dendrobin A, derived from Dendrobium nobile, exhibits significant anti-hepatocellular carcinoma effects. Its anti-cancer mechanism mainly involves inhibiting the NF-κB signaling pathway to suppress tumor cell proliferation, migration, invasion, epithelial-mesenchymal transition, block cell cycle progression, and induce cell apoptosis.


The active compound Dendrobin A, derived from Dendrobium nobile, exhibits significant anti-hepatocellular carcinoma effects. Its anti-cancer mechanism mainly involves inhibiting the NF-κB signaling pathway to suppress tumor cell proliferation, migration, invasion, epithelial-mesenchymal transition, block cell cycle progression, and induce cell apoptosis.

Le texte complet de cet article est disponible en PDF.

Highlights

Dendrobine A from Dendrobium nobile shows promise as an anti-HCC agent due to its multiple anti-cancer properties.
Dendrobine A inhibits the proliferation of HCC cells by arresting the cell cycle at the G2-M phase.
Dendrobine A induces apoptosis and inhibits the epithelial-mesenchymal transition of HCC cells.
The anti-HCC effects of Dendrobine A are related to its inhibition of the activation of NF-κB signaling.

Le texte complet de cet article est disponible en PDF.

Keywords : Hepatocellular carcinoma, Dendrobin A, Biological function, mRNA sequencing, NF-κB pathway


Plan


© 2024  The Authors. Publié par Elsevier Masson SAS. Tous droits réservés.
Ajouter à ma bibliothèque Retirer de ma bibliothèque Imprimer
Export

    Export citations

  • Fichier

  • Contenu

Vol 177

Article 117013- août 2024 Retour au numéro
Article précédent Article précédent
  • Preclinical in vivo assessment of the activity of AZD7442 anti-SARS-CoV-2 monoclonal antibodies against Omicron sublineages
  • Jean-Sélim Driouich, Maxime Cochin, Guillaume Lingas, Léa Luciani, Cécile Baronti, Ornéllie Bernadin, Magali Gilles, Paola Mariela Saba Villarroel, Grégory Moureau, Paul-Rémi Petit, Axelle Dupont, Jacques Izopet, Nassim Kamar, Brigitte Autran, Gilles Paintaud, Sophie Caillard, Amandine le Bourgeois, Christophe Richez, Lionel Couzi, Aliénor Xhaard, Zora Marjanovic, Jerome Avouac, Caroline Jacquet, Dany Anglicheau, Morgane Cheminant, Stéphanie Nguyen, Benjamin Terrier, Jacques Eric Gottenberg, Caroline Besson, Sophie Letrou, Josephine Tine, Joe Miantezila Basilua, Denis Angoulvant, Coralie Tardivon, Gilles Blancho, Guillaume Martin-Blondel, Yazdan Yazdanpanah, France Mentré, Vincent Lévy, Franck Touret, Jérémie Guedj, Xavier de Lamballerie, Antoine Nougairède
| Article suivant Article suivant
  • Brusatol alleviates pancreatic carcinogenesis via targeting NLRP3 in transgenic Krastm4Tyj Trp53tm1Brn Tg (Pdx1-cre/Esr1*) #Dam mice
  • Juan Zhang, Yu-Lin Wu, Hong-Xi Xu, Yi-Bo Zhang, Pei-Yao Ren, Yan-Fang Xian, Zhi-Xiu Lin

Bienvenue sur EM-consulte, la référence des professionnels de santé.
L’accès au texte intégral de cet article nécessite un abonnement.

Déjà abonné à cette revue ?

Mon compte


Plateformes Elsevier Masson

Déclaration CNIL

EM-CONSULTE.COM est déclaré à la CNIL, déclaration n° 1286925.

En application de la loi nº78-17 du 6 janvier 1978 relative à l'informatique, aux fichiers et aux libertés, vous disposez des droits d'opposition (art.26 de la loi), d'accès (art.34 à 38 de la loi), et de rectification (art.36 de la loi) des données vous concernant. Ainsi, vous pouvez exiger que soient rectifiées, complétées, clarifiées, mises à jour ou effacées les informations vous concernant qui sont inexactes, incomplètes, équivoques, périmées ou dont la collecte ou l'utilisation ou la conservation est interdite.
Les informations personnelles concernant les visiteurs de notre site, y compris leur identité, sont confidentielles.
Le responsable du site s'engage sur l'honneur à respecter les conditions légales de confidentialité applicables en France et à ne pas divulguer ces informations à des tiers.


Tout le contenu de ce site: Copyright © 2024 Elsevier, ses concédants de licence et ses contributeurs. Tout les droits sont réservés, y compris ceux relatifs à l'exploration de textes et de données, a la formation en IA et aux technologies similaires. Pour tout contenu en libre accès, les conditions de licence Creative Commons s'appliquent.