Denis C, Paris H, Murat J C
Biochem J. 1986 Nov 1;239(3):531-6. doi: 10.1042/bj2390531.
Vasoactive intestinal peptide (VIP) was found to cause a dose-dependent decrease in fructose 2,6-bisphosphatase concomitant with an increase in cyclic AMP in cultured HT29 cancer cells from human colon. The maximum effect was a 41% decrease obtained with 10 nM-VIP, and half-maximum effect was obtained with 0.75 nM-VIP. The effect of 2.5 nM-VIP was almost totally counteracted (i.e. fructose 2,6-bisphosphate concentration was restored) by either adrenaline (1 microM) or the alpha 2-adrenergic agonist UK-14304 (1 microM); the alpha 2-agonist clonidine (1 microM) was less efficient, since the VIP effect was decreased by 72% only. The adrenaline effect was totally antagonized by 1 microM-yohimbine. It is concluded that, in the HT29 cancer cells, the fructose 2,6-bisphosphate-producing system is sensitive to variations of cyclic AMP concentration and is under the dual control of VIP and alpha 2-adrenergic receptors.
研究发现,血管活性肠肽(VIP)可导致人结肠来源的HT29培养癌细胞中果糖2,6 - 二磷酸酶呈剂量依赖性降低,同时细胞内环磷酸腺苷(cAMP)水平升高。最大效应是10 nM - VIP导致果糖2,6 - 二磷酸酶降低41%,半最大效应是0.75 nM - VIP时出现。2.5 nM - VIP的效应几乎完全被肾上腺素(1 μM)或α2 - 肾上腺素能激动剂UK - 14304(1 μM)抵消(即果糖2,6 - 二磷酸浓度恢复);α2 - 激动剂可乐定(1 μM)的效果较差,因为它只能使VIP的效应降低72%。1 μM育亨宾可完全拮抗肾上腺素的作用。研究得出结论,在HT29癌细胞中,果糖2,6 - 二磷酸生成系统对cAMP浓度变化敏感,且受VIP和α2 - 肾上腺素能受体的双重调控。