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首页> 外文期刊>Biochemical Pharmacology >Modulating phosphate consumption, a novel therapeutic approach for the control of cancer cell proliferation and tumorigenesis
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Modulating phosphate consumption, a novel therapeutic approach for the control of cancer cell proliferation and tumorigenesis

机译：调节磷酸盐消耗，一种用于控制癌细胞增殖和肿瘤发生的新的治疗方法

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摘要

Phosphorus, often in the form of inorganic phosphate (Pi), is critical to cellular function on many levels; it is required as an integral component of kinase signaling, in the formation and function of DNA and lipids, and energy metabolism in the form of ATP. Accordingly, crucial aspects of cell mitosis - such as DNA synthesis and ATP energy generation - elevate the cellular requirement for Pi, with rapidly dividing cells consuming increased levels. Mechanisms to sense, respond, acquire, accumulate, and potentially seek Pi have evolved to support highly proliferative cellular states such as injury and malignant transformation. As such, manipulating Pi availability to target rapidly dividing cells presents a novel strategy to reduce or prevent unrestrained cell growth. Currently, limited knowledge exists regarding how modulating Pi consumption by pre-cancerous cells might influence the initiation of aberrant growth during malignant transformation, and if reducing the bioavailability or suppressing Pi consumption by malignant cells could alter tumorigenesis. The concept of targeting Pi-regulated pathways and/or consumption by pre-cancerous or tumor cells represents a novel approach to cancer prevention and control, although current data remains insufficient as to rigorously assess the therapeutic value and physiological relevance of this strategy. With this review, we present a critical evaluation of the paradox of how an element critical to essential cellular functions can, when available in excess, influence and promote a cancer phenotype. Further, we conjecture how Pi manipulation could be utilized as a therapeutic intervention, either systemically or at the cell level, to ultimately suppress or treat cancer initiation and/or progression.
机译：磷通常以无机磷酸盐（PI）的形式，对许多级别的细胞功能至关重要;需要作为激酶信号传导的整体组分，在DNA和脂质的形成和功能中，以及ATP形式的能量代谢。因此，细胞分子病的关键方面 - 例如DNA合成和ATP能量产生 - 提高PI的细胞需求，迅速分裂的细胞消耗增加的水平。感知，响应，获取，积累和潜在寻求PI的机制已经发展起来支持高增殖的细胞状态，例如损伤和恶性转化。因此，操纵PI可用性以瞄准快速分区的细胞提出了一种新的策略来减少或防止无拘无束的细胞生长。目前，有关癌细胞预癌细胞的调节PI消耗的调节可能影响有限的知识可能影响恶性转化期间的异常生长，并且如果降低生物利用度或抑制恶性细胞的PI消耗可能会改变肿瘤发生。靶向PI调节途径和/或肿瘤细胞消耗的概念代表了一种新的癌症预防和控制方法，尽管目前的数据仍然不足以严格评估该策略的治疗价值和生理相关性。通过本综述，我们对悖论的关键评估涉及对本质细胞功能至关重要的元素，当可用过量，影响和促进癌症表型时。此外，我们猜测PI操纵如何作为治疗介入，其系统或在细胞层中可以用作治疗介入，最终抑制或治疗癌症起始和/或进展。

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