伤口愈合与癌症干细胞：炎症作为乳腺癌治疗耐药性的驱动因素
Wound healing and cancer stem cells: inflammation as a driver of treatment resistance in breast cancer.
作者信息
Arnold Kimberly M, Opdenaker Lynn M, Flynn Daniel, Sims-Mourtada Jennifer
机构信息
Center for Translational Cancer Research, Helen F. Graham Cancer Center, Christiana Care Health Services, Inc., Newark, DE, USA. ; Department of Medical Laboratory Sciences, University of Delaware, Newark, DE, USA.
Center for Translational Cancer Research, Helen F. Graham Cancer Center, Christiana Care Health Services, Inc., Newark, DE, USA. ; Department of Biological Sciences, University of Delaware, Newark, DE, USA.
出版信息
Cancer Growth Metastasis. 2015 Jan 29;8:1-13. doi: 10.4137/CGM.S11286. eCollection 2015.
The relationship between wound healing and cancer has long been recognized. The mechanisms that regulate wound healing have been shown to promote transformation and growth of malignant cells. In addition, chronic inflammation has been associated with malignant transformation in many tissues. Recently, pathways involved in inflammation and wound healing have been reported to enhance cancer stem cell (CSC) populations. These cells, which are highly resistant to current treatments, are capable of repopulating the tumor after treatment, causing local and systemic recurrences. In this review, we highlight proinflammatory cytokines and developmental pathways involved in tissue repair, whose deregulation in the tumor microenvironment may promote growth and survival of CSCs. We propose that the addition of anti-inflammatory agents to current treatment regimens may slow the growth of CSCs and improve therapeutic outcomes.
伤口愈合与癌症之间的关系早已为人所知。调节伤口愈合的机制已被证明可促进恶性细胞的转化和生长。此外，慢性炎症与许多组织中的恶性转化有关。最近，有报道称炎症和伤口愈合相关通路可增加癌症干细胞（CSC）群体。这些细胞对当前治疗具有高度抗性，能够在治疗后使肿瘤重新生长，导致局部和全身复发。在本综述中，我们重点介绍了参与组织修复的促炎细胞因子和发育通路，其在肿瘤微环境中的失调可能促进癌症干细胞的生长和存活。我们建议在当前治疗方案中添加抗炎药物可能会减缓癌症干细胞的生长并改善治疗效果。
Zotero 插件