ArticleAmerican journal of cancer research2025
Placental mesenchymal stem cell-derived interleukin-6 promotes neuroblastoma progression.
Article in American journal of cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Neuroblastoma (NB) is a prevalent pediatric malignancy, yet the role of mesenchymal stem cells (MSCs) in NB progression remains unclear. MSCs are known to secrete various cytokines, including interleukin (IL)-6, and their influence on NB cells and tumor xenografts were investigated in this study. Placenta-derived mesenchymal stem cells (PMSCs) were isolated from chorionic villi and characterized via flow cytometry. The obtained PMSCs were co-cultured with NB cells or IL-6-silenced PMSCs. Comprehensive assays were conducted to assess proliferation, colony formation, cell cycle progression, apoptosis, migration, invasion, and epithelial-mesenchymal transition (EMT). RNA-seq identified differentially expressed genes (DEGs) in NB cells, predominantly enriched in Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathways (P < 0.05). qRT-PCR revealed elevated levels of IL-6 and other oncogenic cytokines in PMSCs (P < 0.05). In vivo, IL-6 knockdown in PMSCs significantly suppressed NB xenograft growth, accompanied by reduced expression of Ki-67, proliferating cell nuclear antigen (PCNA), Caspase 9, and Snail as shown by immunohistochemistry (P < 0.05). Western blotting confirmed activation of phosphatidylinositol 3-kinases/protein kinase B (PI3K/AKT) pathway in NB cells after co-culture with PMSCs, which was attenuated by PI3K inhibition. Notably, IL-6 knockdown markedly suppressed NB xenograft progression and downregulated associated signaling markers (P < 0.05). Collectively, PMSC-derived IL-6 potentiates NB progression via PI3K-AKT signaling, presenting a potential therapeutic target in neuroblastoma.
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