Department of Thoracic, Head and Neck Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Unit 950, Houston, Texas 77030, USA.
Department of Gynecologic Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Unit 950, Houston, Texas 77030, USA.
Nat Commun. 2013;4:2427. doi: 10.1038/ncomms3427.
The miR-200 family is well known to inhibit the epithelial-mesenchymal transition, suggesting it may therapeutically inhibit metastatic biology. However, conflicting reports regarding the role of miR-200 in suppressing or promoting metastasis in different cancer types have left unanswered questions. Here we demonstrate a difference in clinical outcome based on miR-200's role in blocking tumour angiogenesis. We demonstrate that miR-200 inhibits angiogenesis through direct and indirect mechanisms by targeting interleukin-8 and CXCL1 secreted by the tumour endothelial and cancer cells. Using several experimental models, we demonstrate the therapeutic potential of miR-200 delivery in ovarian, lung, renal and basal-like breast cancers by inhibiting angiogenesis. Delivery of miR-200 members into the tumour endothelium resulted in marked reductions in metastasis and angiogenesis, and induced vascular normalization. The role of miR-200 in blocking cancer angiogenesis in a cancer-dependent context defines its utility as a potential therapeutic agent.
miR-200 家族是众所周知的抑制上皮-间充质转化,这表明它可能通过治疗抑制转移生物学。然而,miR-200 在不同癌症类型中抑制或促进转移的作用存在相互矛盾的报告,这使得一些问题仍未得到解答。在这里,我们根据 miR-200 在阻断肿瘤血管生成中的作用展示了临床结果的差异。我们证明 miR-200 通过直接和间接机制抑制血管生成,通过靶向肿瘤内皮细胞和癌细胞分泌的白细胞介素-8 和 CXCL1。通过使用几种实验模型,我们证明了 miR-200 通过抑制血管生成在卵巢癌、肺癌、肾癌和基底样乳腺癌中的治疗潜力。将 miR-200 成员递送至肿瘤内皮细胞可显著减少转移和血管生成,并诱导血管正常化。miR-200 在阻断依赖于癌症的血管生成中的作用定义了其作为一种潜在治疗剂的效用。