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首页> 外文期刊>Cell cycle >Cell death of MCF-7 human breast cancer cells induced by EGFR activation in the absence of other growth factors.
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Cell death of MCF-7 human breast cancer cells induced by EGFR activation in the absence of other growth factors.

机译:在没有其他生长因子的情况下,由EGFR激活诱导的MCF-7人乳腺癌细胞的细胞死亡。

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摘要

The epidermal growth factor (EGF) receptor (EGFR) plays an important role in the growth and progression of breast cancer. Overexpression of EGFR or the high activity of EGFR signal pathway has been related with increases in cell proliferation and a poor prognosis in patients with breast cancer. Several human breast cancer cell lines depend on estrogen for their proliferation. EGF may bypass the requirement of estrogen for the proliferation of breast cancer cells. To evaluate this hypothesis, MCF-7 breast cancer cells were stimulated with EGF and the effects on cell proliferation, signal pathways, and cell cycle progression were determined. The results demonstrate that EGF stimulation in the absence of others growth factors induced a modest effect on cell proliferation and the induction of a cellular arrest in the G(1) phase of the cell cycle. Although phosphorylation of AKT and ERK proteins were detected, this phosphorylation was insufficient to support of cell cycle progression. Cellular arrest in G(1) phase was accompanied by an increase in p21(CIP1) protein, down regulation of the BCL-2 protein, induction of caspase-8, and ARHI/NOEY2 an imprinted tumor suppressor gene. These results indicate that EGFR activation by itself is not sufficient for the proliferation of breast cancer cells and suggest the existence of a mechanism that induces apoptosis upon EGFR activation.
机译:表皮生长因子(EGF)受体(EGFR)在乳腺癌的生长和进展中起着重要作用。 EGFR的过表达或EGFR信号通路的高活性与乳腺癌患者的细胞增殖增加和预后不良有关。几种人类乳腺癌细胞系依赖雌激素进行增殖。 EGF可能绕过雌激素对乳腺癌细胞增殖的需求。为了评估该假设,用EGF刺激MCF-7乳腺癌细胞,并确定其对细胞增殖,信号通路和细胞周期进程的影响。结果表明,在没有其他生长因子的情况下,EGF刺激可诱导适度的细胞增殖,并诱导细胞周期G(1)期的细胞停滞。尽管检测到AKT和ERK蛋白的磷酸化,但这种磷酸化不足以支持细胞周期进程。在G(1)期细胞停滞伴随着p21(CIP1)蛋白的增加,BCL-2蛋白的下调,caspase-8的诱导和ARHI / NOEY2(一种印迹的抑癌基因)的出现。这些结果表明,EGFR激活本身不足以促进乳腺癌细胞的增殖,并且表明存在在EGFR激活时诱导凋亡的机制的存在。

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