| First Author | Coppo R | Year | 2021 |
| Journal | Cancer Lett | Volume | 510 |
| Pages | 13-23 | PubMed ID | 33862151 |
| Mgi Jnum | J:316900 | Mgi Id | MGI:6715778 |
| Doi | 10.1016/j.canlet.2021.04.005 | Citation | Coppo R, et al. (2021) ESDN inhibits melanoma progression by blocking E-selectin expression in endothelial cells via STAT3. Cancer Lett 510:13-23 |
| abstractText | 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. |
