Abstract

Abstract Leukocyte Cell-Derived Chemotaxin 2 (LECT2) protein is expressed preferentially in the liver in a constitutive manner and secreted into bloodstream. Recently studies indicate that LECT2 potentially associated with the liver injury, repair, and regeneration, but other functions are still unknown. Angiogenesis is a process of new blood vessel formation which has essential roles in development, repair, tumor growth, invasion, and metastasis. In our previous studies, we have recently identified LECT2 as a potential tumor suppressor, correlating with decreased vascular invasion in hepatocellular carcinomas (HCC). In this study, we evaluated the function of recombinant LECT2 (rLECT2) proteins on angiogenesis by using human umbilical vein endothelial cells (HUVEC). We demonstrated a selective and significant inhibition of VEGF165-induced angiogenic activity in HUVEC by rLECT2 protein through inhibiting the proliferation, migration, and tube formation. The rLECT2 protein also suppressed VEGF165-induced angiogenesis in CAM assay and matrigel plug assay. Otherwise, we use different stage of HCC to evaluate the density, amounts, and volumes of blood vessels are associated with LECT2 protein level. Furthermore, we also evaluate the association between LECT2 protein level and the maturity of blood vessels. In conclusion, we for the first time found that LECT2 play an important role in anti-angiogenesis. Moreover, the LECT2 might have broad therapeutic applications in diseases characterized by excessive angiogenesis. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5302. doi:1538-7445.AM2012-5302

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