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- W3153810008 abstract "An interactive crosstalk between tumor and stroma cells is essential for metastatic melanoma progression. We evidenced that ESDN/DCBLD2/CLCP1 plays a crucial role in endothelial cells during the spread of melanoma. Precisely, increased extravasation and metastasis formation were revealed in ESDN-null mice injected with melanoma cells, even if the primary tumor growth, vessel permeability, and angiogenesis were not enhanced. Interestingly, improved adhesion of melanoma cells to ESDN-depleted endothelial cells was observed, due to the presence of higher levels of E-selectin transcripts/proteins in ESDN-defective cells. In accordance with these results, anticorrelation was observed between ESDN and E-selectin in human endothelial cells. Most importantly, our data revealed that cimetidine, an E-selectin inhibitor, was able to block cell adhesion, extravasation, and metastasis formation in ESDN-null mice, underlying a major role of ESDN in E-selectin transcription upregulation, which according to our data, may presumably be linked to STAT3. Based on our results, we propose a protective role for ESDN during the spread of melanoma and reveal its therapeutic potential." @default.
- W3153810008 created "2021-04-26" @default.
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- W3153810008 date "2021-07-01" @default.
- W3153810008 modified "2023-10-17" @default.
- W3153810008 title "ESDN inhibits melanoma progression by blocking E-selectin expression in endothelial cells via STAT3" @default.
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- W3153810008 doi "https://doi.org/10.1016/j.canlet.2021.04.005" @default.
- W3153810008 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8581997" @default.
- W3153810008 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/33862151" @default.
- W3153810008 hasPublicationYear "2021" @default.
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