Smith K B, Losonczy I, Sahai A, Pannerselvam M, Fehnel P, Salomon D S
J Cell Physiol. 1983 Oct;117(1):91-100. doi: 10.1002/jcp.1041170113.
Epidermal growth factor (EGF) inhibited the growth of A431 human epidermoid carcinoma cells. The tumor promoting, phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA) also retarded A431 cell growth. Addition of both TPA and EGF inhibited cell growth in an additive or synergistic manner depending upon the initial plating density of the cultures. EGF increased the production of diacylglycerol (60-70%) and stimulated the synthesis of phosphatidylinositol (PI) from 3H-inositol (three- to fourfold increase). Both of these responses were attenuated in the presence of TPA. TPA alone stimulated the production of diacylglycerol (DG) but had little effect on PI synthesis. The biological effect of TPA appeared to be mediated by the presence of a high-affinity receptor for phorbol esters on A431 cells. Moreover, the binding of 125I-EGF to A431 cells was unaffected by TPA, suggesting that the antagonistic effects of TPA were occurring distal to the EGF receptor. These findings also indicated that although TPA and EGF both inhibited A431 cell growth, this effect could be dissociated from changes in PI synthesis but may be dependent upon transient changes in DG production.
表皮生长因子（EGF）抑制A431人表皮样癌细胞的生长。促肿瘤的佛波酯12 - O - 十四酰佛波醇 - 13 - 乙酸酯（TPA）也会延缓A431细胞的生长。根据培养物的初始接种密度，同时添加TPA和EGF会以相加或协同的方式抑制细胞生长。EGF增加了二酰基甘油的产生（60 - 70%），并刺激了由3H - 肌醇合成磷脂酰肌醇（PI）（增加三到四倍）。在TPA存在的情况下，这两种反应均减弱。单独的TPA刺激二酰基甘油（DG）的产生，但对PI合成影响很小。TPA的生物学效应似乎是由A431细胞上存在佛波酯的高亲和力受体介导的。此外，125I - EGF与A431细胞的结合不受TPA影响，这表明TPA的拮抗作用发生在EGF受体的下游。这些发现还表明，尽管TPA和EGF都抑制A431细胞生长，但这种效应可能与PI合成的变化无关，而可能取决于DG产生的短暂变化。
