LECT2 (leukocyte cell-derived chemotaxin-2), also known as Chondromodulin-II, is a neutrophil chemotactic protein predominantly expressed in the liver [1]. It was first identified in the heparin-binding components extracted from fetal bovine epiphyseal cartilage [2]. Human LECT2 cDNA encodes a 151 amino acid (aa) precursor that includes an 18 aa signal sequence [3]. The mature human LECT2 is a 16 kDa secreted hepatic protein that has a putative peptidase-M23 domain [3, 4]. Human LECT2 shares 87% and 86% aa sequence identity with mouse and rat LECT2, respectively. LECT2 stimulates the growth and matrix formation of chondrocytes in vitro [2, 5, 6]. In MC3T3-E1 cells, it promotes proliferation but inhibits alkaline phosphatase activity [5, 6]. In vivo study suggested LECT2 can directly suppress the development of type II collagen antibody–induced arthritis [4]. Recent studies have shown that LECT2 is an important regulator of tumor growth during hepatocellular carcinoma development and progression; it inhibits the angiogenic effect of HUVECs in vitro and in vivo [7].
Reference
[1]. Yamagoe, S. et al. (1996) Immunol. Lett. 52:9.
[2]. Hiraki, Y. et al. (1996) J. Bio. Chem. 271:22657.
[3]. Slowik, V. and U. Apte (2017) Clin. Transl. Sci. 10:249.
[4]. Okumura, A. et al. (2013) FEBS Lett. 587:404.
[5]. Mori, Y. et al. (1997) FEBS Letters 406:310.
[6]. Shukunami, C. et al. (1999) J. Biochem. 125:436.
[7]. Chen, C.K. et al. (2016) Sci. Rep. 6:31398.