1009 A role for auxiliary TGF-beta receptor endoglin as a modulator of tumor progression

Pérez-Gómez, Eduardo; Villa‐Morales, María; Santos, Joyce Nascimento dos; Fernández‐Piqueras, José; Bernabéu, Carmelo; Quintanilla, Miguel

doi:10.1016/s1359-6349(09)70302-7

Cited by 1 publication

(1 citation statement)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Another interesting observation in the SCC patient samples that were analyzed, was increased endoglin expression by VSCC cells with spindle morphology compared to the conventional VSCC cells. Strikingly, it was previously shown in mouse keratinocytes that endoglin shedding induces a spindle cell phenotype (50), while in VSCC, expression seems prominent on the spindle phenotype SCC cells. Importantly, vulvar spindle cell morphology is associated with a worse prognosis than conventional VSCC (10).…”

Section: Discussionmentioning

confidence: 87%

Endoglin and squamous cell carcinomas

et al. 2023

View full text Add to dashboard Cite

Despite the fact that the role of endoglin on endothelial cells has been extensively described, its expression and biological role on (epithelial) cancer cells is still debatable. Especially its function on squamous cell carcinoma (SCC) cells is largely unknown. Therefore, we investigated SCC endoglin expression and function in three types of SCCs; head and neck (HNSCC), esophageal (ESCC) and vulvar (VSCC) cancers. Endoglin expression was evaluated in tumor specimens and 14 patient-derived cell lines. Next to being expressed on angiogenic endothelial cells, endoglin is selectively expressed by individual SCC cells in tumor nests. Patient derived HNSCC, ESCC and VSCC cell lines express varying levels of endoglin with high interpatient variation. To assess the function of endoglin in signaling of TGF-β ligands, endoglin was overexpressed or knocked out or the signaling was blocked using TRC105, an endoglin neutralizing antibody. The endoglin ligand BMP-9 induced strong phosphorylation of SMAD1 independent of expression of the type-I receptor ALK1. Interestingly, we observed that endoglin overexpression leads to strongly increased soluble endoglin levels, which in turn decreases BMP-9 signaling. On the functional level, endoglin, both in a ligand dependent and independent manner, did not influence proliferation or migration of the SCC cells. In conclusion, these data show endoglin expression on individual cells in the tumor nests in SCCs and a role for (soluble) endoglin in paracrine signaling, without directly affecting proliferation or migration in an autocrine manner.

show abstract

Section: Discussionmentioning

confidence: 87%