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. 2020 May 15;10:727. doi: 10.3389/fonc.2020.00727

Figure 2.

Figure 2

The relationship between IGFBP3 and IGFBP7. IGF bioavailability is determined by sequestration in (ternary) complexes with IGFBP3 and ALS in the circulation, or in (binary) complexes with IGFBP3 in the cell environment. IGFBP7 binding partners are insulin, IGF-I, and activin, the levels of which can be controlled by retinoic acid and TGF-β. The function of IGFBP7 and IGFBP3 may be a double-edged sword in cancer proliferation, prognosis, and survival. The molecular mechanisms for IGFBP7 and IGFBP3 suppression of cancer remain to be fully elucidated, but some studies indicate that the primary mechanisms involve promoter methylation and the regulation of p21. ALS: Acid labile subunit; IGF: insulin-like growth factor; IGFBP7: IGF binding protein 7; IGF-1R: IGF-1 receptor; INSR: insulin receptor; IRS: insulin receptor substrate; MAPK: mitogen-activated protein kinase; mTOR: mammalian target of rapamycin; Shc: Src homology 2 domain-containing; TGF: transforming growth factor. As cancer cells are shown (histological inset), osteosarcoma cells show anaplastic cytological features associated with osteoid formation.