摘要
disintegrin和metalloprotease(亚当)17 sheddase,能够释放ectodomains膜蛋白,如生长因子(如表皮生长因子受体配体),细胞因子及其受体、粘附和信号分子。这些活动调节多种生理和病理过程包括炎症、肿瘤的生长和转移过程。在本文中,我们将总结ADAM17生物学和关注它在癌症中的作用和可能的使用ADAM17抑制剂在癌症治疗。最近的成就在这一领域的发展包括小分子metalloprotease ADAM17与增强特异性抑制剂,单克隆抗体,合成短RNA分子基因沉默。这些方法成功地抑制癌细胞的生长和侵袭性或致敏细胞毒性药物,电离辐射或靶向治疗,在临床前研究。这些发现表明ADAM17抑制剂的重新定位,这还没有被证明失败作为抗炎剂,为新的抗癌治疗的发展,尤其是在EGFR ligand-dependent癌症。未来的研究应该解决ADAM17抑制剂作为短期治疗结合不同的抗癌疗法。
关键词: ADAM17、癌症、小分子抑制剂
Current Drug Targets
Title:Targeting ADAM17 Sheddase Activity in Cancer
Volume: 17 Issue: 16
Author(s): Armando Rossello, Elisa Nuti, Silvano Ferrini, Marina Fabbi
Affiliation:
关键词: ADAM17、癌症、小分子抑制剂
摘要: A disintegrin and metalloprotease (ADAM)17 is a sheddase, capable of releasing the ectodomains of membrane proteins such as growth factors (e.g. Epidermal Growth Factor Receptor ligands), cytokines and their receptors, adhesion and signaling molecules. These activities regulate several physiological and pathological processes including inflammation, tumor growth and metastatic progression. In this review, we will summarize ADAM17 biology and focus on its role in cancer and the possible usage of ADAM17 inhibitors in cancer therapy. Recent achievements in this area include the development of small molecule metalloprotease inhibitors with enhanced specificity for ADAM17, monoclonal antibodies, and synthetic short RNA molecules for gene silencing. These approaches successfully inhibited cancer cell growth and invasiveness or sensitized them to cytotoxic drugs, ionizing radiations or targeted therapies, in preclinical studies. These findings suggest the repositioning of ADAM17 inhibitors, which have yet proven unsuccessful as anti-inflammatory agents, for the development of new anti-cancer therapies, particularly in EGFR ligand-dependent cancers. Future studies should address ADAM17 inhibitors as short-term treatments in combination with different anti-cancer therapies.
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Armando Rossello, Elisa Nuti, Silvano Ferrini, Marina Fabbi , Targeting ADAM17 Sheddase Activity in Cancer, Current Drug Targets 2016; 17 (16) . https://dx.doi.org/10.2174/1389450117666160727143618
DOI https://dx.doi.org/10.2174/1389450117666160727143618 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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