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Obvious neovascularization is a key feature of hepatocellular carcinoma(HCC) and the status of neovascularization in HCC is closely correlated with thetumor growth and patient prognosis. The actual effect of current antivasculartreatment including embolization to HCC is not satisfactory. Compensatory angiogenesisis one of the primary causes responsible for failure of antiangiogenic therapy.Bone marrow-derived endothelial progenitor cells (BM-EPCs) are considered as importantbuilding blocks for adult neovascularization. However, the role of mobilized BM-EPCsin HCC remains unknown. In this study, GFP+-BM orthotropic HCC mice were establishedto investigate whether BM-EPCs are involved in HCC-induced neovascularization.We found that a large number of BM-EPCs were mobilized into the circulation withthe development of HCC, recruited into the HCC region and incorporated into thevascular endothelium directly by differentiation into vascular endothelial cells,including sinus, capillary vessels and great vessels. Dynamic observation revealedthat the mobilization and the incorporation of BM-EPCs into different types ofvessels were present in early phases and throughout the whole process of HCC growth.The proportion of BM-EPCs in vessels increased gradually, from 17 to 21% withtumor growth. Moreover, injected GFP+-EPCs also specifically homed to tumor tissueand incorporated into tumor vessels directly. In this initial study, we demonstratedthat BM-EPCs play a prominent role in HCC neovascularization. Blockade of BM-EPC-mediatedvasculogenesis may improve the efficacy of current anti-vascularization therapyfor patients with HCC.

oncology reports

The mobilization, recruitment and contribution of bone marrow-derived endothelial progenitor cells to the tumor neovascularization occur at an early stage and throughout the entire process of hepatocellular carcinoma growth