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The insulin family consists of insulin, insulin-like growth factor 1 (IGF-1), insulin-like growth factor 2 (IGF-2), their receptors (IR, IGF-1R and IGF-2R), and their binding proteins. All three ligands are involved in cell proliferation, apoptosis, protein synthesis and metabolism due to their homologous sequences and structural similarities. Insulin-like growth factor 2, a member of the insulin family, plays an important role in embryonic development, metabolic disorders, and tumorigenesis by combining with three receptors with different degrees of affinity.

Insulin-like growth factor 2 (IGF-2 IGF-II) is a member of the insulin family of polypeptide growth factors, which are involved in development and growth. It is an imprinted gene, expressed only from the paternal allele, and epigenetic changes at this locus are associated with Wilms tumor, Beckwith-Wiedemann syndrome, rhabdomyosarcoma, and Silver-Russell syndrome. IGF-2 IGF-II is a mediator of prolactin-induced alveologenesis; prolactin, IGF-2, and cyclin D1, all of which are overexpressed in breast cancers, are components of a developmental pathway in the mammary gland. IGF-2 and exhibited statistically significant, positive associations with colorectal cancer risk when cases were confined to those diagnosed within a relatively short period after enrolment. Circulating IGF-2 and IGFBP-3 can serve as early indicators of impending colorectal cancer. IGF-2 IGF-II appears to be involved in the progression of many tumors. It binds to at least two different types of receptors: IGF type 1 (IGF 1R) and mannose 6-phosphate IGF type 2 (M6-P IGF 2R). Ligand binding to IGF 1R provokes mitogenic and anti-apoptotic effects. M6-P IGF 2R has a tumor suppressor function—it mediates IGF 2 degradation. Mutation of M6-P IGF 2R causes both diminished growth suppression and augmented growth stimulation. This study aimed to investigate the role of IGF 2 and its receptors (IGF 1R and IGF 2R) in human gastric cancer.