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dc.contributor.authorRado, Mariam
dc.contributor.authorFisher, David
dc.date.accessioned2022-07-07T09:26:05Z
dc.date.available2022-07-07T09:26:05Z
dc.date.issued2022
dc.identifier.citationRado, M., & Fisher, D. (2022). The paracrine effect of hypoxic and normoxic cancer secretion on the proliferation of brain endothelial cells (bend.3). Cells, 11(7), 1197. https://doi.org/10.3390/cells11071197en_US
dc.identifier.issn2073-4409
dc.identifier.urihttps://doi.org/10.3390/cells11071197
dc.identifier.urihttp://hdl.handle.net/10566/7562
dc.description.abstract: Background: This study aimed to investigate the disruption of cell cycle phases of bEnd.3 cells exposed to cancer paracrine secretion. Cancer cells have been reported to use the secretion of paracrine factors to compromise the endothelial barrier to prepare for their passage into the parenchyma. As cancer cells are known to act differently under conditions of hypoxia, we investigated how conditional media (CM) derived from breast and glioblastoma cells incubated under conditions of normoxia and hypoxia would affect proliferation of brain endothelial cells (bEnd.3). Methods: Brain endothelial cells (bEnd.3) were cultivated with normoxic and hypoxic CM generated from breast cancer MCF7 cells and glioblastoma U-87 cells. Cell proliferation was evaluated using the trypan blue exclusion assay and phases of the cell cycle were evaluated using flow cytometry. Results: bEnd.3 proliferations was suppressed more aggressively with hypoxic CM after 72 and 96 h; cell cycle analysis showed that paracrine treatment tended to prevent BECs from entering the G2 phase, thus suppressing cell division.en_US
dc.language.isoenen_US
dc.publisherMDPIen_US
dc.subjectCell proliferationen_US
dc.subjectBrain endothelial cellen_US
dc.subjectHypoxiaen_US
dc.subjectNormoxiaen_US
dc.subjectCanceren_US
dc.titleThe paracrine effect of hypoxic and normoxic cancer secretion on the proliferation of brain endothelial cells (bend.3)en_US
dc.typeArticleen_US


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