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首页> 外文期刊>Molecular and Cellular Biology >Diltiazem inhibits transferrin receptor expression and causes G1 arrest in normal and neoplastic T cells.
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Diltiazem inhibits transferrin receptor expression and causes G1 arrest in normal and neoplastic T cells.

机译：地尔硫卓抑制运铁蛋白受体的表达并导致正常和肿瘤性T细胞中的G1阻滞。

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Transferrin receptor expression is essential for the proliferation of both normal and malignant T cells. While transferrin receptor expression in normal T cells is tightly coupled to interleukin-2 receptor expression, transferrin receptor expression in malignant cells is usually constitutive and is released from this constraint. Temporally, the appearance of these membrane receptors is preceded by changes in the expression of the proto-oncogenes c-myc and c-myb. In addition, although an increase in the level of intracellular free calcium occurs early in the sequence of T-cell activation, the activation events dependent on this calcium flux have not been resolved. In the present study we report that diltiazem, an ion channel-blocking agent that inhibits calcium influx, arrested the growth in vitro of both normal and malignant human T cells in the G1 phase of the cell cycle. However, diltiazem did not inhibit the expression of c-myc or interleukin-2 receptor mRNA and protein in normal mitogen-activated T cells or the constitutive expression of c-myc and c-myb mRNA in malignant T cells (T acute lymphoblastic leukemia cells). In contrast, diltiazem prevented the induction of transferrin receptor (mRNA and protein) in normal T cells and caused a progressive loss of transferrin receptor (mRNA and protein) in malignant T cells. These data demonstrate that diltiazem can dissociate several growth-related processes normally occurring in G1 and thereby disrupt the biochemical cascade leading to cell proliferation.
机译：转铁蛋白受体的表达对于正常和恶性T细胞的增殖都是必不可少的。正常T细胞中的转铁蛋白受体表达与白介素2受体表达紧密相关，而恶性细胞中的转铁蛋白受体表达通常是组成性的，并不受此限制。暂时地，在这些膜受体出现之前，原癌基因c-myc和c-myb的表达发生变化。另外，尽管细胞内游离钙水平的升高在T细胞活化的顺序中较早发生，但是依赖于该钙通量的活化事件尚未解决。在本研究中，我们报道地尔硫卓是一种抑制钙离子流入的离子通道阻滞剂，在细胞周期的G1期阻止了正常和恶性人类T细胞的体外生长。然而，地尔硫卓不会抑制正常丝裂原激活的T细胞中c-myc或白细胞介素2受体mRNA和蛋白的表达或恶性T细胞（T急性淋巴细胞白血病细胞）中c-myc和c-myb mRNA的组成型表达。 ）。相反，地尔硫卓阻止了正常T细胞中转铁蛋白受体（mRNA和蛋白质）的诱导，并导致了恶性T细胞中转铁蛋白受体（mRNA和蛋白质）的逐渐丧失。这些数据表明地尔硫卓可以使正常情况下在G1中发生的几种与生长相关的过程解离，从而破坏导致细胞增殖的生化级联反应。

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