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Alpha-fetoprotein (AFP) is a tumorous marker for the diagnosis of hepatocellular carcinoma (HCC), it is synthesized mainly by the embryo yolk sac, fetal liver and the gastrointestinal tract [1]. AFP belongs to the family of protein products of albuminoid genes, which are located in tandem arrangement in chromosome 4 (region 4q11-q13) [2]. AFP is a glycoprotein with molecular weight of about 68-73 kDa and carbohydrate content of 3%-5%. Primary structure of full-length human AFP (HAFP) molecule is represented by 609 amino acid (aa) residues from which a signal peptide of 18 aa residues is removed during processing to produce the mature protein of 591 aa residues [3-5]. AFP has multiple ligand-binding sites and a plasma half-life of approximately 3-5 days [6]. Embryo cells internalize the AFP-ligand complex through the AFP receptor (AFPR)-mediated endocytosis, and cancer cells performed the same to internalize the AFP [7]. The AFPR is mostly absent in normal adult cells, except for a small population of regulatory immune cells, such as myeloidderived suppressor cells (MDSCs), specific T cells and monocytes. Selective targeting of MDSCs through AFPbinding receptor was able to inhibit the growth of cancer cells [8-10]. Therefore, AFP and AFPR are not only proteins of nutrient transport system and tumor markers, but also involve in regulating the growth and differentiation of cells, and immune response.

Inhibition of Autophagy and Immune Response: Alpha-fetoprotein Stimulates Initiation of Liver Cancer