Membrane stabilization by intimate contact between cells reduces their Mg2+ activity and suppresses the neoplastic phenotype.
Membrane stabilization by intimate contact between cells reduces their Mg2+ activity and suppresses the neoplastic phenotype.
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DOI：
10.1016/j.semcancer.2004.08.003
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发表时间：
2005-04
影响因子：
14.5
通讯作者：
H. Rubin
中科院分区：
文献类型：
--
作者：
H. Rubin
通过与正常细胞接触使转化细胞正常化的机制被认为与刺激正常接触抑制细胞生长的机制有关。刺激是基于在整个G1期的细胞膜的扰动生长因子。膜扰动的主要效应是细胞内游离Mg2+的长期持续增加，这增加了多肽合成的起始频率并加速了DNA合成的开始。由于转化细胞的质膜保持在持续扰动状态并形成差的细胞间粘附，因此其失去对细胞内Mg 2+活性的控制。然而，在极高密度下最大化转化细胞之间的接触稳定了它们的质膜，降低了它们的Mg 2+含量并使它们的表型正常化。正常化也可以在与较低密度的静止、汇合的正常细胞接触时获得。反对需要连接通信的证据支持膜稳定与恢复Mg2+调节作为正常化的机制。
The mechanism of normalizing transformed cells by contact with normal cells is considered in relation to the mechanism of stimulating the growth of normal contact-inhibited cells. Stimulation is based on perturbation of the plasma membrane throughout the G1 period by growth factors. A primary effect of the membrane perturbation is a long-sustained increase of intracellular free Mg2+which increases the initiation frequency of polypeptide synthesis and accelerates the onset of DNA synthesis. Because the plasma membrane of transformed cells is kept in a continuously perturbed state and forms poor intercellular adhesions, it loses control of intracellular Mg2+activity. However, maximizing contact between transformed cells at extremely high density stabilizes their plasma membrane, lowers their Mg2+content and normalizes their phenotype. Normalization may also be obtained in contact with lower densities of quiescent, confluent normal cells. Evidence against a need for junctional communication supports membrane stabilization with restoration of Mg2+regulation as the mechanism of normalization.