Glipizide suppresses prostate cancer progression in the TRAMP model by inhibiting angiogenesis.
Glipizide suppresses prostate cancer progression in the TRAMP model by inhibiting angiogenesis.
复制标题
格列吡嗪通过抑制血管生成来抑制 TRAMP 模型中前列腺癌的进展
DOI：
10.1038/srep27819
复制
发表时间：
2016-06-13
影响因子：
4.6
通讯作者：
Wang L
中科院分区：
文献类型：
--
作者：
Qi C;Bin Li;Yang Y;Yang Y;Li J;Zhou Q;Wen Y;Zeng C;Zheng L;Zhang Q;Li J;He X;Zhou J;Shao C;Wang L
非癌症药物的药物再利用是开发新癌症疗法的一种有吸引力的方法。使用TRAMP转基因小鼠模型，格列吡嗪，一种广泛使用的2型糖尿病药物，已被确定为抑制前列腺癌（PC）的生长和转移。血管生成与各种人类癌症发展密切相关。有趣的是，格列吡嗪显着降低PC肿瘤组织中的微血管密度，而不抑制前列腺癌细胞增殖的MTT法和流式细胞术研究。此外，格列吡嗪通过调节HMGIY/Angiopoietin-1信号通路抑制人脐静脉内皮细胞管状结构的形成。综上所述，这些结果表明，格列吡嗪有可能被重新利用为一种有效的治疗PC靶向肿瘤诱导的血管生成的治疗。
Drug repurposing of non-cancer drugs represents an attractive approach to develop new cancer therapy. Using the TRAMP transgenic mouse model, glipizide, a widely used drug for type 2 diabetes mellitus, has been identified to suppress prostate cancer (PC) growth and metastasis. Angiogenesis is intimately associated with various human cancer developments. Intriguingly, glipizide significantly reduces microvessel density in PC tumor tissues, while not inhibiting prostate cancer cell proliferation from the MTT assay and flow cytometry investigation. Moreover, glipizide inhibits the tubular structure formation of human umbilical vein endothelial cells by regulating the HMGIY/Angiopoietin-1 signaling pathway. Taken together, these results demonstrate that glipizide has the potential to be repurposed as an effective therapeutic for the treatment of PC by targeting tumor-induced angiogenesis.