Development of technology capable of promoting tissue remodeling without stimulating tissue fibrosis and cancer growth

我们通过比较TG 2 +/+和TG 2-/-小鼠，发现TG 2在肿瘤诱导的血管生成中起重要作用，这些小鼠在发育过程中没有异常表现。我们提供的证据表明，TG 2控制RB蛋白的交联和磷酸化以及E2 F的反式激活，导致诱导EZH 2，EZH 2抑制抗血管生成因子血管抑制素1（VASH 1），从而维持肿瘤血管生成。因此，TG 2及其下游信号分子可能成为抗肿瘤血管生成治疗的新靶点，而不影响组织重塑。

We found an essential role of TG2 in tumor-induced angiogenesis through a comparison between TG2+/+ and TG2-/- mice, which show no abnormal manifestation during development. We provide evidence that TG2 controls crosslinking and phosphorylation of RB proteins and trans-activation of E2F that results in induction of EZH2, which suppresses an anti-angiogenic factor, vasohibin 1 (VASH1), thereby sustaining tumor angiogenesis. Thus, TG2 and under signaling molecules maybe a novel target for anti-angiogenic therapy against cancer, without affecting tissue remodeling.