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组织型转谷氨酰胺酶(tissue transglutaminase,TG2或tTG)作为一种多功能酶在肿瘤的发生和发展过程中通过参与核因子-κB(nuclear factor kappa B,NF-κB)途径和黏着斑激酶(focal adhesion kinase,FAK)/磷脂酰肌醇3-激酶(phosphatidylinositol3 kinase,PI3K)/蛋白激酶B(protein kinaseB,AKT)等途径来维持肿瘤细胞的生长和长期存活,其同时也是肿瘤细胞自噬和凋亡串扰的关键调控因素。TG2通过与细胞外基质相互作用产生黏附效应,同时介导上皮-间质转化(epithelial-mesenchymal transition,EMT)促进肿瘤的侵袭和转移。表皮生长因子受体(epidermal growth factor receptor,EGFR)和基质金属蛋白酶(matrix metalloproteinases,MMPs)调控的侵袭和转移信号通路也依赖于TG2的作用。本综述重点阐述了TG2在肿瘤发生、发展、侵袭和转移中的作用及其可能的作用机制,以期为肿瘤治疗的新方法提供一些宝贵的思路。
Tissue transglutaminase (TG2 or tTG) acts as a multifunctional enzyme in tumorigenesis and progression through its involvement in the nuclear factor-kappa B (NF-κB) pathway and focal adhesion kinase (FAK) / phosphatidylinositol 3 kinase (PI3K) / protein kinase B (AKT) and other pathways to maintain tumor cell growth and long-term survival, which is also the tumor cell autophagy And the key regulatory factors of apoptosis crosstalk. TG2 has an adhesion effect through the interaction with the extracellular matrix, and at the same time it mediates epithelial-mesenchymal transition (EMT) to promote tumor invasion and metastasis. The invasion and metastasis signaling pathways regulated by epidermal growth factor receptor (EGFR) and matrix metalloproteinases (MMPs) also depend on the role of TG2. This review focuses on the role of TG2 in tumorigenesis, development, invasion and metastasis, and its possible mechanism of action, with a view to providing some valuable ideas for a new approach to cancer therapy.