ArticleDiscover oncology2025
Visfatin promotes multiple myeloma cell proliferation and inhibits apoptosis by inducing IL-6 production via NF-κB pathways.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Targeting inflammatory microenvironments: overcoming therapy resistance and immunosuppression.Molecular cancer · 2026Review
- Metabolism in Tumour-Induced Bone Disease.Current osteoporosis reports · 2026Review
- The concurrent silencing of Tim-3 and STAT-3 promotes tumor regression both in vitro and in ovo.BMC cancer · 2025Article
- The Role of Visfatin/NAMPT in the Pathogenesis of Psoriasis.Metabolites · 2025Article
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Authors and funding
9 authors.
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Abstract
backgroundMultiple myeloma (MM) is the second most prevalent hematological malignancy that results in the proliferation of malignant plasma cells and the overproduction of monoclonal immunoglobulin. Visfatin plays an important role in the regulation of apoptosis, oxidative stress, and inflammation; however, to this date, the role of visfatin in multiple myeloma is unclear.
objectiveTo explore the role of visfatin in multiple myeloma and find new targets for MM treatment.
methodsIn this study, expression of visfatin in bone marrow was detected by ELISA. The diagnostic value of visfatin was determined by receiver operating characteristic (ROC) curve analysis. After the quality control by performing western blot to confirm the knockdown of visfatin in two MM cell lines, the phenotype (proliferation and apoptosis) of visfatin in MM was determined by carrying out in vitro experiments, including CCK8, flow cytometry, and western blot. Several cytokines were determined by real-time PCR, followed by in vivo experiments and immunohistochemical assays. IκB, NF-κbp65, and phosphorylation were determined by western blot.
resultsWe found that visfatin level increased in the bone marrow of MM patients compared to controls. ROC curve analysis result showed that bone marrow visfatin was able to distinguish MM patients from controls. In vitro and in vivo, visfatin promotes MM cell proliferation. The production of IL-6 was attenuated by visfatin knockdown. Furthermore, we showed that visfatin could activate IL-6 production via the NF-κB signaling pathway.
conclusionsIn MM, visfatin promotes tumor progression by upregulating IL-6 production, which may be a novel therapeutic target for the treatment of MM patients.
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