Youn BuHyun, Kim Hag Dong, Kim Joon
Division of Biological Sciences, Pusan National University, College of Natural Sciences, Busan, 609-735, Korea.
Expert Opin Ther Targets. 2008 Nov;12(11):1419-30. doi: 10.1517/14728222.12.11.1419.
Neo-angiogenesis seems to be a critical feature of breast tumor growth, migration and metastasis. Inhibition of angiogenesis may provide information regarding treatment. Since angiogenesis is the result of complex processes, controlled by several angiogenic (pro- and/or -anti) factors and their receptors, multiple ways to prevent or retrogress tumor-induced angiogenesis have been proposed. The clinically significant activity of bevacizumab and other antiangiogenic treatments have attracted a great deal of interest.
OBJECTIVE/METHODS: We discuss biological aspects of breast cancer angiogenesis and nucleoside diphosphate kinase (NDPK) as a key molecule in this process.
RESULTS/CONCLUSIONS: In clinical and experimental trials, it was reported that NDPK is inversely related to breast cancer metastasis and angiogenesis. To inhibit the metastatic potential of cancer cells, Nm23-H1/NDP kinase appears to interact with many proteins involved in cellular signal transduction in angiogenesis and tumorigenesis, and therefore reduces the activation of the extracellular signal-regulated kinase (ERK)/MAPK in response to those signals.
新血管生成似乎是乳腺肿瘤生长、迁移和转移的关键特征。抑制血管生成可能为治疗提供信息。由于血管生成是复杂过程的结果，受多种血管生成（促血管生成和/或抗血管生成）因子及其受体控制，因此已提出多种预防或逆转肿瘤诱导的血管生成的方法。贝伐单抗和其他抗血管生成治疗的临床显著活性引起了广泛关注。
目的/方法：我们讨论乳腺癌血管生成的生物学方面以及核苷二磷酸激酶（NDPK）作为这一过程中的关键分子。
结果/结论：在临床和实验研究中，有报道称NDPK与乳腺癌转移和血管生成呈负相关。为抑制癌细胞的转移潜能，Nm23-H1/NDP激酶似乎与血管生成和肿瘤发生中许多参与细胞信号转导的蛋白质相互作用，因此减少了细胞外信号调节激酶（ERK）/丝裂原活化蛋白激酶（MAPK）对这些信号的反应性激活。
