Donor HLA mismatch promotes full donor T-cell chimerism in the allogeneic stem cell transplant with reduced-intensity conditioning and post-transplant cyclophosphamide GVHD prophylaxis

Cioccio, Joseph; Rakszawski, Kevin; Zheng, Hong; Nickolich, Myles; Naik, Seema; Wirk, Baldeep; Rybka, Witold B.; Ehmann, Christopher; Silar, Brooke; Vajdic, Caitlin; Shah, Neal; Tuanquin, Leonard; Greiner, Robert; Brown, Valerie I.; Hohl, Raymond J.; Claxton, David F.; Mineishi, Shin; Minagawa, Kentaro; Shike, Hiroko

doi:10.1007/s00277-022-05077-2

Cited by 3 publications

References 33 publications

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Correlation Between Endoglin and Malignant Phenotype in Human Melanoma Cells: Analysis of hsa-mir-214 and hsa-mir-370 in Cells and Their Extracellular Vesicles

Ruíz-Llorente

Ruiz-Rodríguez

Savini

et al. 2023

Advances in Experimental Medicine and Biology

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Endoglin (CD105) is an auxiliary receptor of transforming growth factor (TGF)-β family members that is expressed in human melanomas. It is heterogeneously expressed by primary and metastatic melanoma cells, and endoglin targeting as a therapeutic strategy for melanoma tumors is currently been explored. However, its involvement in tumor development and malignancy is not fully understood. Here, we find that endoglin expression correlates with malignancy of primary melanomas and cultured melanoma cell lines. Next, we have analyzed the effect of ectopic endoglin expression on two miRNAs (hsa-mir-214 and hsa-mir-370), both involved in melanoma tumor progression and endoglin regulation. We show that compared with control cells, overexpression of endoglin in the WM-164 melanoma cell line induces; (i) a significant increase of hsa-mir-214 levels in small extracellular vesicles (EVs) as well as an increased trend in cells; and (ii) significantly lower levels of hsa-mir-370 in the EVs fractions, whereas no significant differences were found in cells. As hsa-mir-214 and hsa-mir-370 are not just involved in melanoma tumor progression, but they can also target endoglin-expressing endothelial cells in the tumor vasculature, these results suggest a complex and differential regulatory mechanism involving the intracellular and extracellular signaling of hsa-mir-214 and hsa-mir-370 in melanoma development and progression.

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