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dc.contributor.authorHaugse, Ragnhild
dc.contributor.authorLanger, Anika
dc.contributor.authorMurvold, Elsa Thodesen
dc.contributor.authorCostea, Daniela Elena
dc.contributor.authorGjertsen, Bjørn Tore
dc.contributor.authorGilja, Odd Helge
dc.contributor.authorKotopoulis, Spiros
dc.contributor.authorRuiz de Garibay, Gorka
dc.contributor.authorMcCormack, Emmet
dc.date.accessioned2021-05-03T12:10:33Z
dc.date.available2021-05-03T12:10:33Z
dc.date.created2020-11-06T10:09:41Z
dc.date.issued2020
dc.identifier.issn1999-4923
dc.identifier.urihttps://hdl.handle.net/11250/2753276
dc.description.abstractThe use of ultrasound (US) and microbubbles (MB), usually referred to as sonoporation, has great potential to increase the efficacy of chemotherapy. However, the molecular mechanisms that mediate sonoporation response are not well-known, and recent research suggests that cell stress induced by US + MBs may contribute to the treatment benefit. Furthermore, there is a growing understanding that the effects of US + MBs are beyond only the cancer cells and involves the tumour vasculature and microenvironment. We treated pancreatic cancer cells (MIA PaCa-2) and stromal cells, fibroblasts (BJ) and human umbilical vein endothelial cells (HUVECs), with US ± MB, and investigated the extent of uptake of cell impermeable dye (calcein, by flow cytometry), viability (cell count, Annexin/PI and WST-1 assays) and activation of a number of key proteins in important intracellular signalling pathways immediately and 2 h after sonoporation (phospho flow cytometry). Different cell types responded differently to US ± MBs in all these aspects. In general, sonoporation induces immediate, transient activation of MAP-kinases (p38, ERK1/2), and an increase in phosphorylation of ribosomal protein S6 together with dephosphorylation of 4E-BP1. The sonoporation stress-response resembles cellular responses to electroporation and pore-forming toxins in membrane repair and restoring cellular homeostasis, and may be exploited therapeutically. The stromal cells were more sensitive to sonoporation than tumoural cells, and further efforts in optimising sonoporation-enhanced therapy should be targeted at the microenvironment.en_US
dc.language.isoengen_US
dc.publisherMDPIen_US
dc.rightsNavngivelse 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/deed.no*
dc.titleLow-Intensity Sonoporation-Induced Intracellular Signalling of Pancreatic Cancer Cells, Fibroblasts and Endothelial Cellsen_US
dc.typeJournal articleen_US
dc.typePeer revieweden_US
dc.description.versionpublishedVersionen_US
dc.rights.holderCopyright 2020 The Authorsen_US
dc.source.articlenumber1058en_US
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1
dc.identifier.doi10.3390/pharmaceutics12111058
dc.identifier.cristin1845512
dc.source.journalPharmaceuticsen_US
dc.identifier.citationPharmaceutics. 2020, 12(11), 1058en_US
dc.source.volume12en_US
dc.source.issue11en_US


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