Melanoma Cell Viability Is Reduced after Endoglin Silencing with Gene Electrotransfer

Tumor angiogenesis represents a promising target for cancer treatment. Tumor endothelial cells proliferate faster than normal endothelial cells due to activation of specific endothelial cell markers. One of them is endoglin, a Transforming Growth Factor

β

(TGF-

β

) co-receptor, involved predominantly in cellular proliferation and migration. Besides the expression of endoglin in tumor endothelial cells, it is also expressed in some types of tumor cells, especially in melanoma. Therefore, in melanoma, targeting endoglin could provide a beneficial therapeutic effect based on simultaneously inhibiting angiogenesis and melanoma cell proliferation. Therefore, the aim of our study was to determine the level of endoglin expression in endothelial and tumor cell lines (melanoma and adenocarcinoma) and to investigate if endoglin expression is associated with changes in cell viability after endoglin silencing. Our study showed that endothelial and melanoma cells express high levels of endoglin and that after endoglin silencing with gene electrotranfer (GET), cell viability was specifically decreased, whereas in tumor cells with low expression of endoglin, only non-specific decrease in cell viability was observed after GET. Our study is one of the first studies exploring the effect of endoglin on biological properties of melanoma cells and indicates new possibilities for melanoma treatment with targeted gene therapy approach.