Instituto de Fisiología, Biología Molecular y Neurociencias (IFIBYNE), CONICET-Universidad de Buenos Aires, Buenos Aires, Argentina; Tumor Biology Program, Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, FL, USA; University of Miami- Center for AIDS Research (UM-CFAR)/Sylvester Comprehensive Cancer Center (CCC) Argentina Consortium for Research and Training in Virally Induced AIDS-Malignancies, University of Miami Miller School of Medicine, Miami, FL, USA; Miami Center for AIDS Research, Department of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, FL, USA.
Tumor Biology Program, Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, FL, USA; University of Miami- Center for AIDS Research (UM-CFAR)/Sylvester Comprehensive Cancer Center (CCC) Argentina Consortium for Research and Training in Virally Induced AIDS-Malignancies, University of Miami Miller School of Medicine, Miami, FL, USA; Miami Center for AIDS Research, Department of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, FL, USA.
Trends Mol Med. 2023 Mar;29(3):188-200. doi: 10.1016/j.molmed.2022.12.003. Epub 2023 Jan 10.
Endothelial-to-mesenchymal transition has been described in tumors as a source of mesenchymal stroma, while the reverse process has been proposed in tumor vasculogenesis and angiogenesis. A human oncogenic virus, Kaposi's sarcoma herpes virus (KSHV), can regulate both processes in order to transit through this transition 'boulevard' when infecting KS oncogenic progenitor cells. Endothelial or mesenchymal circulating progenitor cells can serve as KS oncogenic progenitors recruited by inflammatory cytokines because KSHV can reprogram one into the other through endothelial-to-mesenchymal and mesenchymal-to-endothelial transitions. Through these novel insights, the identity of the potential oncogenic progenitor of KS is revealed while gaining knowledge of the biology of the mesenchymal-endothelial differentiation axis and pointing to this axis as a therapeutic target in KS.
内皮细胞向间充质转化已在肿瘤中被描述为间充质基质的来源，而在肿瘤血管生成和血管生成中则提出了相反的过程。人类致癌病毒卡波济肉瘤疱疹病毒 (KSHV) 可以调节这两个过程，以便在感染 KS 致癌前体细胞时通过这个过渡“林荫大道”。内皮细胞或间充质循环祖细胞可以作为被炎症细胞因子募集的 KS 致癌前体细胞，因为 KSHV 可以通过内皮细胞向间充质和间充质向内皮转化将一种细胞重新编程为另一种细胞。通过这些新的见解，揭示了 KS 的潜在致癌前体细胞的身份，同时也了解了间充质-内皮分化轴的生物学，并将该轴作为 KS 的治疗靶点。
