Coffey R J, Leof E B, Shipley G D, Moses H L
J Cell Physiol. 1987 Jul;132(1):143-8. doi: 10.1002/jcp.1041320120.
Suramin, a polyanionic compound, has previously been shown to dissociate platelet-derived growth factor (PDGF) from its receptor. In the present study suramin was found to inhibit the growth of sparse cultures of AKR-2B cells in fetal bovine serum (FBS)-supplemented medium in a dose-dependent, reversible fashion. Suramin also inhibited the ability of FBS, transforming growth factor beta (TGF beta), heparin-binding growth factor type-2 (HBGF-2), and epidermal growth factor (EGF) to stimulate DNA synthesis in density-arrested cultures of AKR-2B cells. The inhibition of growth factor-stimulated mitogenicity was directly correlated to the dose of suramin required to inhibit the binding of 125I-labeled TGF beta, HBGF-2, and EGF to their cell surface receptors. Suramin affected TGF beta and HBGF-2-related events at a 10-15-fold lower dose than that required for EGF-related events. It was also noted that suramin inhibited TGF beta-stimulated soft agar colony formation of AKR-2B (clone 84A) cells as well as the spontaneous colony formation of AKR-MCA cells, a chemically transformed derivative of AKR-2B cells. This demonstrates that suramin's spectrum of action for growth factors and their receptors should be extended to include TGF beta, HBGF-2, and EGF as well as PDGF. The data further suggest that the spontaneous growth of AKR-MCA cells in soft agar is dependent on growth factor binding to cell surface receptors.
苏拉明是一种多阴离子化合物，先前已被证明能使血小板衍生生长因子（PDGF）与其受体解离。在本研究中，发现苏拉明在补充胎牛血清（FBS）的培养基中以剂量依赖性、可逆的方式抑制AKR - 2B细胞稀疏培养物的生长。苏拉明还抑制FBS、转化生长因子β（TGFβ）、2型肝素结合生长因子（HBGF - 2）和表皮生长因子（EGF）刺激AKR - 2B细胞密度抑制培养物中DNA合成的能力。生长因子刺激的有丝分裂活性的抑制与抑制125I标记的TGFβ、HBGF - 2和EGF与其细胞表面受体结合所需的苏拉明剂量直接相关。苏拉明影响TGFβ和HBGF - 2相关事件的剂量比影响EGF相关事件所需的剂量低10 - 15倍。还注意到苏拉明抑制TGFβ刺激的AKR - 2B（克隆84A）细胞软琼脂集落形成以及AKR - MCA细胞（AKR - 2B细胞的化学转化衍生物）的自发集落形成。这表明苏拉明对生长因子及其受体的作用谱应扩展到包括TGFβ、HBGF - 2、EGF以及PDGF。数据进一步表明，AKR - MCA细胞在软琼脂中的自发生长依赖于生长因子与细胞表面受体的结合。
