VIP ANALOGS INHIBIT SMALL-CELL LUNG-CANCER GROWTH

被引：0
作者：
MOODY, TW
ZIA, F
GOLDSTEIN, AL
NAYLOR, PH
SARIN, E
BRENNEMAN, D
KOROS, AMC
REUBI, JC
KORMAN, LY
FRIDKIN, M
GOZES, I
机构：
[1] NICHHD,NEUROCHEM UNIT,LDN,BETHESDA,MD 20892
[2] UNIV PITTSBURGH,GRAD SCH PUBL HLTH,DEPT INFECT DIS & MICROBIOL,PITTSBURGH,PA 15261
[3] SANDOZ RES INST,CH-3001 BERN,SWITZERLAND
[4] VET ADM MED CTR,GASTROENTEROL SECT,WASHINGTON,DC 20422
[5] WEIZMANN INST SCI,DEPT ORGAN CHEM,IL-76100 REHOVOT,ISRAEL
[6] SACKLER SCH MED,DEPT CHEM PATHOL,TEL AVIV,ISRAEL
来源：
BIOMEDICAL RESEARCH-TOKYO | 1992年 / 13卷
关键词：
D O I：
暂无
中图分类号：
R-3 [医学研究方法]; R3 [基础医学];
学科分类号：
1001 ;
摘要：
The ability of VIP analogues to interact with small cell lung cancer (SCLC) cells was investigated. Specific I-125-VIP binding to SCLC cell line NCI-H209 was inhibited with high affinity by VIP, PACAP, VIPhybrid (VIPhyb) and thymosin alpha1 (THNalpha1) (IC50 = 10, 20, 700 and 10000 nM respectively) but not thymosin beta4. I-125-I-VIP bound specifically to 3 out of 5 SCLC biopsy specimens. VIP but not VIPhyb or THNalpha1 elevated the cAMP levels 4-fold using cell lines NCI-H345 and H209. Also, VIPhyb and THNalpha1 inhibited SCLC growth using a clonagenic assay. These data suggest that VIPhyb and THNalpha1 interact with SCLC cells and inhibit proliferation.
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页码：131 / 135
页数：5
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