Tetsumoto T, Takada K, Amino N, Miyai K
Department of Laboratory Medicine, Osaka University Medical School, Japan.
Biochem Biophys Res Commun. 1988 Dec 15;157(2):605-10. doi: 10.1016/s0006-291x(88)80293-6.
In quiescent rat thyroid (FRTL-5) cells, the B subunit of cholera toxin, which binds to cell surface ganglioside GM1 specifically, alone induced DNA synthesis and markedly enhanced that induced by insulin in serum-free medium. On the other hand, the B subunit inhibited DNA synthesis induced by thyrotropin (TSH). The B subunit did not activate adenylate cyclase and had no effect on the TSH-induced cyclic adenosine 3',5'-monophosphate (cAMP) production. Moreover, the B subunit inhibited DNA synthesis induced by dibutyryl cAMP (Bt2cAMP) or phorbol-12-myristate-13-acetate (PMA). These data demonstrate that the B subunit has both stimulatory and inhibitory effects on DNA synthesis in FRTL-5 cells depending on the presence of other growth factors and that these effects on cell proliferation by the interaction of the B subunit, possibly with cell surface ganglioside GM1, may involve a mechanism independent from the modulation of membrane receptor function through interaction with growth factor receptor.
在静止的大鼠甲状腺（FRTL - 5）细胞中，霍乱毒素的B亚基特异性结合细胞表面神经节苷脂GM1，单独即可诱导DNA合成，并在无血清培养基中显著增强胰岛素诱导的DNA合成。另一方面，B亚基抑制促甲状腺激素（TSH）诱导的DNA合成。B亚基不激活腺苷酸环化酶，对TSH诱导的环磷酸腺苷（cAMP）生成也无影响。此外，B亚基抑制二丁酰cAMP（Bt2cAMP）或佛波醇 - 12 - 肉豆蔻酸酯 - 13 - 乙酸酯（PMA）诱导的DNA合成。这些数据表明，B亚基根据其他生长因子的存在与否，对FRTL - 5细胞中的DNA合成具有刺激和抑制作用，并且B亚基与细胞表面神经节苷脂GM1相互作用对细胞增殖的这些影响，可能涉及一种独立于通过与生长因子受体相互作用调节膜受体功能的机制。
