Monaco M E, Levy B L, Richardson S B
Department of Physiology and Biophysics, New York University Medical Center, NY 10016.
Biochem Biophys Res Commun. 1988 Mar 15;151(2):717-24. doi: 10.1016/s0006-291x(88)80339-5.
The tumor promoter, tetradecanoylphorbolacetate (TPA), causes a significant increase in both insulin secretion and the incorporation of 32Pi into phosphatidylcholine (PC) in RIN insulinoma cells. The peptide hormone, arginine vasopressin (AVP), also stimulates these functions, although to a lesser degree. When added together, the effects on secretion and PC metabolism are synergistic. At the same time, TPA inhibits the AVP-stimulated rise in phosphoinositide (PI) metabolism. Neither phloretin nor tamoxifen, reported to be inhibitors of protein kinase C activity, are able to block the effects of TPA on secretion, although both influence PC metabolism.
肿瘤启动子十四烷酰佛波醇乙酸酯（TPA）可使RIN胰岛素瘤细胞中的胰岛素分泌以及32Pi掺入磷脂酰胆碱（PC）的量显著增加。肽类激素精氨酸加压素（AVP）也能刺激这些功能，不过程度较轻。当两者同时添加时，对分泌和PC代谢的影响具有协同作用。同时，TPA可抑制AVP刺激引起的磷酸肌醇（PI）代谢增加。尽管根皮素和他莫昔芬都能影响PC代谢，但据报道它们是蛋白激酶C活性的抑制剂，均无法阻断TPA对分泌的影响。
