Abstract 3382: The roles of leukocyte cell-derived chemotaxin 2 (LECT2) in hepatocellular carcinoma invasion and metastasis

Abstract

Abstract Vascular invasion is the major poor prognostic factor in hepatocellular carcinoma (HCC) progression, and the overall five year survival is only 40-50%. To elucidate the molecular pathogenesis of HCC, using high throughput technology suppression subtractive hybridization (SSH) and transmembrane/secreted protein (TMS) oligonucleotide microarray, we found that leukocyte cell-derived chemotaxin 2 (LECT2) correlated with low vascular invasion. Human LECT2 is a 16-kDa basic protein and specifically expressed in adult and fetal livers. However, its biological function has not been identified. Here, we show that LECT2 level was significantly reverse-correlated with vascular invasion, high tumor stage, early recurrence, and poor survival. LECT2 overexpression did not influence HCC cells growth property, but strongly reduced migration and invasion in vitro assay. LECT2 suppressed tumor growth, intrahepatic, and lung metastasis in orthotopic liver transplantation mice. The mechanism of LECT2 inhibited HCC cells invasion and metastasis might be mediated via affected multiple receptor tyrosine kinases. Taken together, these findings indicated that LECT2 suppress the invasiveness and suggest the feasibility of LECT2 expression as a promising prognostic molecular marker for HCC. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3382.