Cell adhesion-mediated radioresistance revisited
Cell adhesion-mediated radioresistance revisited
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DOI：
10.1080/09553000701694335
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发表时间：
2007-01-01
影响因子：
2.6
通讯作者：
Cordes, N.
中科院分区：
文献类型：
--
作者：
Sandfort, V.;Koch, U.;Cordes, N.
目的：在体外研究中，整合素介导的细胞与细胞外基质蛋白的粘附调节细胞对电离辐射的反应。这一机制可能在一定程度上导致肿瘤细胞的放射和化疗耐药表型。材料和方法：检索PubMed数据库，并对数据进行总结，重点关注细胞粘附介导的辐射抵抗（CAM-RR）。结果：整合素及其相关的下游信号通路以及整合素与受体酪氨酸激酶的协同相互作用介导了防御机制，加剧了放疗对肿瘤细胞的治疗性根除。结论：更好地了解被称为局灶黏附的多蛋白、多功能细胞-基质相互作用介导复合物的分子组成和功能，可能会指出正常细胞和肿瘤细胞之间的显著差异，这可能会促进放射治疗中新型靶向治疗的发展。
Purpose: Integrin-mediated adhesion of cells to proteins of the extracellular matrix modulates the cellular response to ionizing radiation in vitro. This mechanism might be in part causative for radiation and chemoresistance phenotypes in tumor cells.Materials and methods: A PubMed database search was performed and the data were summarized with a focus on cell adhesion-mediated radioresistance ( CAM-RR).Results: Integrins and their associated downstream signaling pathways as well as cooperative interactions of integrins with receptor tyrosine kinases mediate defensive mechanisms that aggravate the therapeutic eradication of tumor cells by radiotherapy.Conclusions: A better knowledge of the molecular composition and function of the multiprotein, multifunctional cell-matrix interactions mediating complexes termed focal adhesions may point at significant differences between normal and tumor cells, which could foster the development of novel targeted therapies in radiotherapy.