ArticleJournal of oncology2023
Multiple Myeloma Side Population Cells Promote Dexamethasone Resistance of Main Population Cells through Exosome Metastasis of LncRNA SNHG16.
Article in Journal of oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Extracellular vesicles in multiple myeloma: pathogenesis and therapeutic application.The FEBS journal · 2025Review
- Sunitinib-resistant renal cell carcinoma cell-derived exosomes promote facilitation of tumor progression via secretion of the lncRNA SNHG16.Human cell · 2025Article
- Therapeutically Harnessing Tumor Cell-Derived Extracellular Vesicles for Multiple Myeloma: Recent Advances and Future Perspectives.Pharmaceutics · 2024Review
- Exosomal lncRNAs as diagnostic and therapeutic targets in multiple myeloma.Frontiers in oncology · 2024Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The emergence of dexamethasone (Dex) resistance limits its efficacy. Side population (SP) cells in MM have strong tumorigenicity. Nevertheless, the detailed effect by which SP cells regulate Dex resistance in MP cells has not been completely verified and needs to be further investigated. Methods: SP and MP cells were sorted from RPMI-8226. mRNA expression and cell viability were analyzed using quantitative real-time PCR (qRT-PCR) and MTS assays, respectively. The presence of exosomal lncRNA SNHG16 was verified by transmission electron microscopy, differential ultracentrifugation, and qRT-PCR. Protein expression levels were measured using western blotting. Gain or loss function analyses were performed to demonstrate the role of SNHG16 in the Dex resistance of MP cells. Results: Dex resistance of SP cells was remarkably stronger than that of MP cells. Compared with MP cells, the survival rate and Dex resistance of MP cells cotreated with SP cell-derived exosomes were increased. SNHG16 expression was significantly enhanced in SP cell-derived exosomes compared to MP cell-derived exosomes. SNHG16 expression was remarkably increased in MP cells transfected with OE-SNHG16 vectors, and Dex resistance of MP cells was enhanced. When SNHG16 was silenced in SP cells, the SNHG16 expression was downregulated in both SP cells and SP cell-derived exosomes. SNHG16 expression and Dex resistance were both remarkably downregulated in MP cells treated with SP-si-SNHG16-exosomes compared to MP cells treated with SP-si-NC-exosomes. Conclusion: MM SP cells promote Dex resistance in MP cells through exosome metastasis of SNHG16.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.