干扰炎症反应：阻断乳腺癌自我更新和进展的新策略？
Interfering with inflammation: a new strategy to block breast cancer self-renewal and progression?
机构信息
Dept. of Oncological Sciences, Molecular Biotechnology Center, University of Turin, Via Nizza 52, Turin, Italy.
出版信息
Breast Cancer Res. 2010;12(2):305. doi: 10.1186/bcr2563. Epub 2010 Apr 28.
Abstract
Two recent studies show that epigenetics and inflammation play a relevant role in the regulation of transformation and cancer cell self-renewal in breast tumours, opening up the possibility that cancer progression can be controlled by interfering with inflammation cascades. Struhl's group showed that transient activation of the Src oncoprotein induces transformation and self-renewal of immortal cells via an epigenetic switch involving NF-kappaB, Lin28, Let-7 microRNA and IL-6. Concomitantly, Wicha's laboratory developed a strategy to selectively target cancer stem cells, retarding tumour growth and reducing metastasis by blocking the IL-8 receptor CXCR1 using either an inhibitor, repertaxin or a specific blocking antibody.
摘要
两项最近的研究表明，表观遗传学和炎症在调节乳腺癌中的转化和癌细胞自我更新中起着重要作用，这为通过干扰炎症级联来控制癌症进展提供了可能性。Struhl 的研究小组表明，Src 癌蛋白的瞬时激活通过涉及 NF-κB、Lin28、Let-7 微 RNA 和 IL-6 的表观遗传开关诱导永生化细胞的转化和自我更新。与此同时，Wicha 的实验室开发了一种策略，通过使用抑制剂 repertaxin 或特异性阻断抗体阻断 IL-8 受体 CXCR1，选择性地靶向癌症干细胞，从而减缓肿瘤生长并减少转移。
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