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首页> 外文期刊>Cytokine >Transforming growth factor (TGF)-beta in conjunction with H-ras activation promotes malignant progression of MCF10A breast epithelial cells.
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Transforming growth factor (TGF)-beta in conjunction with H-ras activation promotes malignant progression of MCF10A breast epithelial cells.

机译：转化生长因子（TGF）-β与H-ras激活一起促进MCF10A乳腺上皮细胞的恶性进展。

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摘要

To address how transforming growth factor (TGF)-beta and oncogenic H-ras signal transduction pathways interact with each other in the malignant progression of breast epithelial cells, we investigated the role of TGF-beta signaling pathway in invasive and migrative properties of H-ras-transformed MCF10A human breast epithelial cells in this study. Here we show that TGF-beta treatment significantly enhanced invasion and migration of H-ras MCF10A cells. H-ras-mediated activation of p38 MAPK and ERK-1/2 was stimulated by TGF-beta. TGF-beta increased expression of matrix metalloproteinase (MMP)-2 through transcriptional activation while TGF-beta-stimulated MMP-9 up-regulation did not occur at transcription level. Activation of p38 MAPK pathway was required for TGF-beta-induced cell migration, invasion and MMP-2/-9 up-regulation, indicating a critical role of p38 MAPK signaling in TGF-beta-promoted tumor progression of H-ras-activated cells. ERKs signaling was also crucial for TGF-beta-enhanced invasive and migrative phenotypes but the up-regulation of MMP-2/-9 was not dependent on ERKs activity. Taken together, we show that TGF-beta promotes H-ras-mediated cell migration and invasive phenotypes in which p38 MAPK and ERKs signaling pathways are involved. Our findings revealing how H-ras and TGF-beta signal pathways interact with each other in MCF10A human breast cells may provide an insight into molecular mechanisms for contribution of TGF-beta to a malignant progression of breast cancer in collaboration with activated H-ras.
机译：为了探讨转化生长因子（TGF）-β和致癌性H-ras信号转导途径在乳腺上皮细胞恶性进展中如何相互作用，我们研究了TGF-β信号通路在H-的侵袭和迁移特性中的作用。 ras转化的MCF10A人乳腺上皮细胞在这项研究中。在这里，我们显示TGF-β治疗显着增强了H-ras MCF10A细胞的侵袭和迁移。 TGF-β刺激H-ras介导的p38 MAPK和ERK-1 / 2的激活。 TGF-β通过转录激活增加了基质金属蛋白酶（MMP）-2的表达，而TGF-β刺激的MMP-9上调在转录水平上没有发生。 TGF-β诱导的细胞迁移，侵袭和MMP-2 / -9上调需要激活p38 MAPK通路，这表明p38 MAPK信号传导在TGF-β促进的H-ras激活的肿瘤进展中起关键作用细胞。 ERKs信号对于TGF-β增强的侵袭和迁移表型也至关重要，但是MMP-2 / -9的上调并不取决于ERKs的活性。两者合计，我们表明TGF-β促进H-ras介导的细胞迁移和侵入性表型，其中涉及p38 MAPK和ERKs信号通路。我们的发现揭示了MCF10A人乳腺细胞中H-ras和TGF-β信号通路如何相互作用，可能与活化H-ras协同作用，揭示了TGF-β对乳腺癌恶性进展的分子机制。

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