Biddle W, Leong S S, Horoszewicz J, Ambrus J L
Proc Soc Exp Biol Med. 1984 Dec;177(3):487-90. doi: 10.3181/00379727-177-3-rc1.
It was suggested that the antitumor effect of the interferons is based in part on their ability to stimulate increased cAMP production. We have explored the interaction of human fibroblastic beta interferon (HFIF) with a cAMP decomposition inhibitory pyrimido-pyrimidine derivative, Mopidamole (RA-233) in cultures of neoplastic and normal cell lines. Mopidamole potentiated the growth inhibitory effect of HFIF in cultures of ES-1 malignant melanoma cells, LNCaP prostatic carcinoma cells, RT-4 transitional carcinoma cells, HT-29 colon adenocarcinoma cells and in diploid fibroblast cells.
有人提出,干扰素的抗肿瘤作用部分基于它们刺激细胞内cAMP生成增加的能力。我们研究了人成纤维细胞β干扰素(HFIF)与一种cAMP分解抑制性嘧啶并嘧啶衍生物潘生丁(RA-233)在肿瘤细胞系和正常细胞系培养物中的相互作用。在ES-1恶性黑色素瘤细胞、LNCaP前列腺癌细胞、RT-4移行癌细胞、HT-29结肠腺癌细胞以及二倍体成纤维细胞的培养物中,潘生丁增强了HFIF的生长抑制作用。