Yao C Z
Zhonghua Wai Ke Za Zhi. 1989 Jan;27(1):42-4, 62.
The molecular biological mechanism of the inhibition by VIP (vasoactive intestinal peptide) on proliferation of pancreatic cancer cells was studied by identifying hormone receptor and using tumor model in vivo. Inhibition appears only in those cells with VIP receptor. Cell-membrane receptors may change during carcinogenesis process. The inhibition of VIP (at certain concentration) on proliferation of tumor cells is remarkable, but, on the other hand, negligible on that of normal cells. These results suggested the feasibility of clinical application of VIP to the treatment of human pancreatic cancer.
通过鉴定激素受体并利用体内肿瘤模型,研究了血管活性肠肽(VIP)对胰腺癌细胞增殖的抑制作用的分子生物学机制。抑制作用仅出现在具有VIP受体的细胞中。细胞膜受体在致癌过程中可能会发生变化。VIP(在一定浓度下)对肿瘤细胞增殖的抑制作用显著,但另一方面,对正常细胞的抑制作用可忽略不计。这些结果提示了VIP临床应用于治疗人类胰腺癌的可行性。