Chen Y, Chen Q, Lu G, Fan Z, Zhong S
Division of Gastroenterology, PUMC Hospital, Beijing.
Chin Med Sci J. 1994 Dec;9(4):215-9.
In the present study, the effects of VIP on the growth of two human pancreatic carcinoma cell lines PU-PAN-1 and PANC-1 were determined using tritiated thymidine incorporation. VIP receptors, intracellular cAMP and polyamines were investigated. The results indicated that VIP at a concentration of 10(-8) mol/L to 10(-7) mol/L can significantly stimulate the growth of PU-PAN-1 cells but not PANC-1 cells. This effect is dose-dependent and abolished by VIP receptor antagonist, [4-C1-Phe6, Leu17] VIP, suggesting VIP receptors in PU-PAN-1 cells may mediate this effect. VIP can markedly elevate the levels of intracellular cAMP and polyamines in PU-PAN-1 cells, indicating that the growth-promoting effect stimulated by VIP may be via a rapid increase in the biosyntheses of cAMP and polyamines. In addition, the VIP-antibody inhibited the growth of PU-PAN-1 cells in serum-free culture medium. The results above suggested that VIP has an autocrine regulatory effect on this pancreatic carcinoma cell line (PU-PAN-1).
在本研究中，使用氚标记的胸腺嘧啶核苷掺入法测定了血管活性肠肽（VIP）对两种人胰腺癌细胞系PU-PAN-1和PANC-1生长的影响。研究了VIP受体、细胞内环磷酸腺苷（cAMP）和多胺。结果表明，浓度为10^(-8) mol/L至10^(-7) mol/L的VIP可显著刺激PU-PAN-1细胞的生长，但对PANC-1细胞无此作用。这种作用呈剂量依赖性，且可被VIP受体拮抗剂[4-C1-苯丙氨酸6，亮氨酸17]VIP消除，提示PU-PAN-1细胞中的VIP受体可能介导了这一作用。VIP可显著提高PU-PAN-1细胞内cAMP和多胺的水平，表明VIP刺激的促生长作用可能是通过cAMP和多胺生物合成的快速增加实现的。此外，VIP抗体在无血清培养基中抑制了PU-PAN-1细胞的生长。上述结果提示，VIP对该胰腺癌细胞系（PU-PAN-1）具有自分泌调节作用。
