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Status: Bibliographieeintrag

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Verfasst von:Kingreen, Tim [VerfasserIn]   i
 Kewitz-Hempel, Stefanie [VerfasserIn]   i
 Rohde, Christian [VerfasserIn]   i
 Hause, Gerd [VerfasserIn]   i
 Sunderkötter, Cord [VerfasserIn]   i
 Gerloff, Dennis [VerfasserIn]   i
Titel:Extracellular vesicles from highly invasive melanoma subpopulations increase the invasive capacity of less invasive melanoma cells through mir-1246-mediated inhibition of CCNG2
Verf.angabe:Tim Kingreen, Stefanie Kewitz-Hempel, Christian Rohde, Gerd Hause, Cord Sunderkötter and Dennis Gerloff
E-Jahr:2024
Jahr:16 September 2024
Umfang:13 S.
Illustrationen:Illustrationen, Diagramme
Fussnoten:Gesehen am 18.02.2025
Titel Quelle:Enthalten in: Cell communication and signaling
Ort Quelle:London : Biomed Central, 2003
Jahr Quelle:2024
Band/Heft Quelle:22(2024), 1, Artikel-ID 442, Seite 1-13
ISSN Quelle:1478-811X
Abstract:Invasive growth is a critical process in tumor progression, requiring the activation of various molecular processes in tumor cells at the invasive front. Intercellular communication between heterogeneous tumor cells enhances cellular activation and adaptation to specific microenvironments. One mechanism of intercellular communication is the delivery of miRNAs through tumor cell-derived extracellular vesicles (EVs). In this context we have observed that conditioned media from a highly invasive cell subpopulation (BLM-HI) enhances the invasive capacity of the parental cell line (BLM). Therefore, we hypothesized that this complex change of cellular behavior is influenced by EV-transported miRNAs. The treatment of BLM cells with EVs derived from BLM-HI cells resulted in a significantly enhanced invasive capacity, as observed in Matrigel-embedded spheroids and in 2D Boyden chamber assays, with a dose-dependent effect. Conversely, the invasive capacity of BLM cells was reduced when secretion of EVs was inhibited by a sphingomyelinase inhibitor. To investigate the molecular mechanisms behind this effect, we performed next-generation sequencing and identified an enrichment of miR-1246 in these EVs. In functional analyses we demonstrated that both the EV mediated delivery of miR-1246 as well as overexpression contributes to the enhanced invasiveness of BLM cells. We identified a binding site of miR-1246 in the 3’UTR of cyclin G2 (CCNG2) and demonstrated direct binding by a luciferase reporter assay.
DOI:doi:10.25673/117114
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

kostenfrei: Resolving-System: https://doi.org/10.25673/117114
 kostenfrei: Volltext: https://doi.org/10.1186/s12964-024-01820-6
 kostenfrei: Volltext: https://biosignaling.biomedcentral.com/articles/10.1186/s12964-024-01820-6
 DOI: https://doi.org/10.25673/117114
 DOI: https://doi.org/10.1186/s12964-024-01820-6
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:Extracellular vesicles
 Invasion
 Melanoma
 miRNAs
K10plus-PPN:1906010226
Verknüpfungen:→ Zeitschrift

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