Cancer stem cells: potential target for bioactive food components.
Cancer stem cells: potential target for bioactive food components.
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DOI：
10.1016/j.jnutbio.2012.03.002
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发表时间：
2012-07
期刊：
影响因子：
--
通讯作者：
Milner JA
中科院分区：
文献类型：
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作者：
Kim YS;Farrar W;Colburn NH;Milner JA
癌症干细胞通常具有与正常干细胞相似的表型和功能特征，包括自我更新和分化的性质。最近的研究结果表明，不受控制的自我更新可能解释癌症复发，并可能代表癌症预防的关键目标。可以想象，由于不适当地食用特定食物及其成分而导致的调节分子的丢失可能会促进癌症干细胞的异常自我更新。事实上，越来越多的证据表明，该网络将自我更新的信号从细胞外区室传递到细胞核，包括干细胞环境的变化，microRNA的诱导表达，增生的核染色质结构，以及分化过程的开/关，作为生物活性食物成分的可能作用位点。不同的膳食成分，如维生素A和D，染料木素，（−）-表没食子儿茶素-3-没食子酸酯（EGCG），萝卜硫素，姜黄素，胡椒碱，茶氨酸和胆碱已被证明可以改变癌症干细胞的自我更新特性。这些生物活性食物成分通过调节网络中的关键反馈分子（包括dickkopf 1（DKK-1）、分泌型卷曲相关蛋白2（sFRP 2）、B细胞特异性莫洛尼鼠白血病病毒整合位点1（Bmi-1）和细胞周期蛋白依赖性激酶6（CDK 6））来影响增殖细胞和静止细胞之间的平衡的能力可能解释了它们的生物反应。总体而言，对食物成分的反应似乎不是组织或器官特异性的，这表明可能存在共同的细胞机制。毫无疑问，需要更多的研究来阐明这些饮食成分在预防肿瘤细胞对传统药物的耐药性和癌症复发方面的生理作用。
Cancer stem cells often have phenotypic and functional characteristics similar to normal stem cells including the properties of self-renewal and differentiation. Recent findings suggest that uncontrolled self-renewal may explain cancer relapses and may represent a critical target for cancer prevention. It is conceivable that the loss of regulatory molecules resulting from inappropriate consumption of specific foods and their constituents may foster the aberrant self-renewal of cancer stem cells. In fact, increasing evidence points to the network delivering signals for self-renewal from extracellular compartments to the nucleus including changes in stem cell environments, inducible expression of microRNAs, hyperplastic nuclear chromatin structures, and the on/off of differentiation process as possible sites of action for bioactive food components. Diverse dietary constituents such as vitamins A and D, genistein, (−)-epigallocatechin-3-gallate (EGCG), sulforaphane, curcumin, piperine, theanine, and choline have been shown to modify self-renewal properties of cancer stem cells. The ability of these bioactive food components to influence the balance between proliferative and quiescent cells by regulating critical feedback molecules in the network including dickkopf 1 (DKK-1), secreted frizzled-related protein 2 (sFRP2), B-cell-specific Moloney murine leukemia virus integration site 1 (Bmi-1), and cyclin-dependent kinase 6 (CDK6) may account for their biological response. Overall, the response to food components does not appear to be tissue or organ specific, suggesting there may be common cellular mechanisms. Unquestionably, additional studies are needed to clarify the physiological role of these dietary components in preventing the resistance of tumor cells to traditional drugs and cancer recurrence.