ArticleExperimental and therapeutic medicine2022
Resibufogenin inhibits the malignant characteristics of multiple myeloma cells by blocking the PI3K/Akt signaling pathway.
Article in Experimental and therapeutic medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- A narrative review of cinobufacini for endometrial cancer: mechanisms and therapeutic implications.Translational cancer research · 2026Review
- Resibufogenin protects against atherosclerosis in ApoEJournal of advanced research · 2026Article
- RNA-Based Therapeutic Strategies in Multiple Myeloma: From Molecular Targets to Delivery and Clinical Translation.International journal of molecular sciences · 2026Review
- Exploring the pharmacological mechanisms of resibufogenin in castration-resistant prostate cancer via network pharmacology and experimental validation.Frontiers in oncology · 2026Article
- Cardiac Glycosides: From Natural Defense Molecules to Emerging Therapeutic Agents.Biomolecules · 2025Review
- Article
- Resibufogenin: An Emerging Therapeutic Compound with Multifaceted Pharmacological Effects - A Comprehensive Review.Medical science monitor : international medical journal of experimental and clinical research · 2024Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Resibufogenin (RBG) is an active ingredient of toad venom that also has antitumor potential. The present study aimed to investigate the role of RBG in multiple myeloma (MM) and the underlying action mechanism involving the PI3K/Akt signaling pathway. A human MM cell line, RPMI8226, was treated with RBG and/or insulin-like growth factor 1 (IGF-1; an activator of the PI3K/AKT signaling pathway). Cell viability and apoptosis were detected using Cell Counting Kit-8 and flow cytometry, respectively. Cell migration and invasion were detected using a Transwell assay. In addition, the epithelial-mesenchymal transition (EMT)-associated proteins (E-cadherin, N-cadherin and Vimentin) and the PI3K/AKT pathway-associated proteins [AKT, phosphorylated (p)-AKT, PI3K and p-PI3K] were measured using western blotting. RBG inhibited the viability, migration and invasion, and promoted the apoptosis of RPMI8226 cells in a dose-dependent manner. RBG at concentrations of 4 and 8 µM upregulated E-cadherin, and downregulated N-cadherin and Vimentin in RPMI8226 cells. RBG also decreased the protein expression of p-AKT and p-PI3K in a dose-dependent manner. In addition, the intervention of IGF-1 weakened the inhibitory effects of RBG on the malignant characteristics of MM cells. RBG-induced inhibition of EMT and the PI3K/AKT pathway were also weakened by IGF-1 treatment. In conclusion, RBG inhibited viability, migration, invasion and EMT, and promoted the apoptosis of MM cells by blocking the PI3K/AKT signaling pathway.
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