UCSF Helen Diller Family Comprehensive Cancer Center, University of California at San Francisco, California 94143-0512, USA.
Int J Biol Sci. 2012;8(7):964-78. doi: 10.7150/ijbs.4564. Epub 2012 Jul 12.
Many advanced tumors produce excessive amounts of Transforming Growth Factor-β (TGF-β) which, in normal epithelial cells, is a potent growth inhibitor. However, in oncogenically activated cells, the homeostatic action of TGF-β is often diverted along alternative pathways. Hence, TGF-β signaling elicits protective or tumor suppressive effects during the early growth-sensitive stages of tumorigenesis. However, later in tumor development when carcinoma cells become refractory to TGF-β-mediated growth inhibition, the tumor cell responds by stimulating pathways with tumor progressing effects. At late stages of malignancy, tumor progression is driven by TGF-β overload. The tumor microenvironment is a target of TGF-β action that stimulates tumor progression via pro-tumorigenic effects on vascular, immune, and fibroblastic cells. Bone is one of the richest sources of TGF-β in the body and a common site for dissemination of breast cancer metastases. Osteoclastic degradation of bone matrix, which accompanies establishment and growth of metastases, triggers further release of bone-derived TGF-β. This leads to a vicious positive feedback of tumor progression, driven by ever increasing levels of TGF-β released from both the tumor and bone matrix. It is for this reason, that pharmaceutical companies have developed therapeutic agents that block TGF-β signaling. Nonetheless, the choice of drug design and dosing strategy can affect the efficacy of TGF-β therapeutics. This review will describe pre-clinical and clinical data of four major classes of TGF-β inhibitor, namely i) ligand traps, ii) antisense oligonucleotides, iii) receptor kinase inhibitors and iv) peptide aptamers. Long term dosing strategies with TGF-β inhibitors may be ill-advised, since this class of drug has potentially highly pleiotropic activity, and development of drug resistance might potentiate tumor progression. Current paradigms for the use of TGF-β inhibitors in oncology have therefore moved towards the use of combinatorial therapies and short term dosing, with considerable promise for the clinic.
许多晚期肿瘤会产生大量转化生长因子-β(TGF-β),而在正常上皮细胞中,TGF-β是一种有效的生长抑制剂。然而,在致癌基因激活的细胞中,TGF-β的体内平衡作用往往会沿着替代途径转移。因此,TGF-β信号在肿瘤发生的早期生长敏感阶段会产生保护或肿瘤抑制作用。然而,在肿瘤发展的后期,当癌细胞对 TGF-β介导的生长抑制产生抗性时,肿瘤细胞会通过具有肿瘤进展作用的途径做出反应。在恶性肿瘤的晚期,肿瘤进展是由 TGF-β过载驱动的。肿瘤微环境是 TGF-β作用的靶点,它通过对血管、免疫和成纤维细胞的促肿瘤生成作用来刺激肿瘤进展。骨骼是体内 TGF-β最丰富的来源之一,也是乳腺癌转移扩散的常见部位。破骨细胞对骨基质的降解,伴随着转移的建立和生长,会进一步触发骨源性 TGF-β的释放。这导致了一个由 TGF-β释放驱动的肿瘤进展的恶性循环,肿瘤和骨基质都会不断释放 TGF-β。正是出于这个原因,制药公司已经开发出了能够阻断 TGF-β信号的治疗药物。尽管如此,药物设计和剂量策略的选择会影响 TGF-β治疗的疗效。本综述将描述四大类 TGF-β抑制剂的临床前和临床数据,即 i)配体陷阱,ii)反义寡核苷酸,iii)受体激酶抑制剂和 iv)肽适体。长期使用 TGF-β抑制剂的策略可能并不明智,因为这类药物具有潜在的高度多效性,并且药物耐药性的发展可能会促进肿瘤进展。因此,目前在肿瘤学中使用 TGF-β抑制剂的范例已经转向了联合治疗和短期用药,这为临床带来了很大的希望。