Rapamycin是经由一种复活岛土壤中的细菌Streptomyces hygroscopicus所分离出的物质，研究发现Rapamycin具有抗生素(杀死细菌)、免疫抑制及抗肿瘤的作用。目前，美国食品与药物管理局已经核准Rapamycin用作防止身体产生器官或骨髓移植排斥反应的药物，同时也可以用于心脏支架的涂层中。
在一篇发表于4月1 日Cancer Research中的研究，科学家们发现Rapamycin还可以防止烟草造成的小鼠肺部肿瘤发展。
研究人员让小鼠暴露于常见的烟草特殊致癌物质一个星期，发现以rapamycin处理的小鼠，体内肿瘤的数量减少了百分之90，而且肿瘤大小减少了百分之74。
Rapamycin是mTOR分子(mammalian Target of Rapamycin)抑制剂。mTOR是一种激酶(serine/threonine kinase)，对于细胞分裂、生长扮演着重要的调节作用，其主要功能为细胞增生讯号之传递，及细胞周期的进行。
mTOR分子接收来自上游(细胞膜表面生长因子及其受体)的讯息，它扮演着相当重要的角色，mTOR分子活化后，可以带动下游一系列的细胞讯息传递，进一步促使细胞产生分化或分裂。而在肿瘤细胞，这样的调节机制出现了异常，导致肿瘤细胞不正常增生及分化不良，因此，mTOR分子是抗癌药物的理想目标。
Rapamycin 已经在实验室中被证实可抑制许多癌细胞的生长，包括横纹肌肉瘤、神经母细胞瘤、肺小细胞癌、骨癌、胰脏癌、乳癌、摄护腺癌、白血病癌细胞及B细胞淋巴癌等。
(资料来源 : biocompare)
部分英文原文：
Cancer Research 67, 3475-3482, April 1, 2007. Published Online First March 27, 2007;
Epidemiology and Prevention
Oral Consumption of Pomegranate Fruit Extract Inhibits Growth and Progression of Primary Lung Tumors in Mice
Naghma Khan1, Farrukh Afaq1, Mee-Hyang Kweon1, KyungMann Kim2 and Hasan Mukhtar1
1 Department of Dermatology and 2 Biostatistics and Medical Informatics, University of Wisconsin Paul P. Carbone Comprehensive Cancer Center, University of Wisconsin-Madison, Madison, Wisconsin
Requests for reprints: Hasan Mukhtar, Department of Dermatology, University of Wisconsin-Madison, Medical Sciences Center, B-25, 1300 University Avenue, Madison, WI 53706. Phone: 608-263-3927; Fax: 608-263-5223; E-mail: hmukhtar@wisc.edu .
To develop novel mechanism-based preventive approaches for lung cancer, we examined the effect of oral consumption of a human achievable dose of pomegranate fruit extract (PFE) on growth, progression, angiogenesis, and signaling pathways in two mouse lung tumor protocols. Benzo(a)pyrene [B(a)P] and N-nitroso-tris-chloroethylurea (NTCU) were used to induce lung tumors, and PFE was given in drinking water to A/J mice. Lung tumor yield was examined on the 84th day and 140 days after B(a)P dosing and 240 days after NTCU treatment. Mice treated with PFE and exposed to B(a)P and NTCU had statistically significant lower lung tumor multiplicities than mice treated with carcinogens only. Tumor reduction was 53.9% and 61.6% in the B(a)P + PFE group at 84 and 140 days, respectively, compared with the B(a)P group. The NTCU + PFE group had 65.9% tumor reduction compared with the NTCU group at 240 days. Immunoblot analysis and immunohistochemistry were used to determine effect on cell survival pathways and markers of cellular proliferation and angiogenesis. PFE treatment caused inhibition of (a) activation of nuclear factor-B and IB kinase, (b) degradation and phosphorylation of IB, (c) phosphorylation of mitogen-activated protein kinases (extracellular signal-regulated kinase 1/2, c-Jun NH2-terminal kinase 1/2, and p38), (d) phosphatidylinositol 3-kinase (p85 and p110), (e) phosphorylation of Akt at Thr308, (f) activation of mammalian target of rapamycin signaling, (g) phosphorylation of c-met, and (h) markers of cell proliferation (Ki-67 and proliferating cell nuclear antigen) and angiogenesis (inducible nitric oxide synthase, CD31, and vascular endothelial growth factor) in lungs of B(a)P- and NTCU-treated mice. Thus, our data show that PFE significantly inhibits lung tumorigenesis in A/J mice and merits investigation as a chemopreventive agent for human lung cancer. [Cancer Res 2007;67(7):3475–82]
