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首页> 外文期刊>Molecular and Cellular Pharmacology >Differential Expression of Key Signaling Proteins in MCF10 Cell Lines, a Human Breast Cancer Progression Model
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Differential Expression of Key Signaling Proteins in MCF10 Cell Lines, a Human Breast Cancer Progression Model

机译：人乳腺癌进展模型MCF10细胞系中关键信号蛋白的差异表达

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Normal 0 false false false EN-US X-NONE X-NONE /* Style Definitions */ table.MsoNormalTable {mso-style-name:"Table Normal"; mso-tstyle-rowband-size:0; mso-tstyle-colband-size:0; mso-style-noshow:yes; mso-style-priority:99; mso-style-parent:""; mso-padding-alt:0in 5.4pt 0in 5.4pt; mso-para-margin:0in; mso-para-margin-bottom:.0001pt; mso-pagination:widow-orphan; font-size:10.0pt; font-family:"Times New Roman","serif";} Breast cancer is a heterogeneous disease that develops through a multistep process whose molecular basis remains poorly understood. The molecular mechanisms of breast cancer progression have been extensively studied using the MCF10 model. We summarized recent results on differential expression of proteins in the MCF10 cell series – MCF10A, MCF10AT1, MCF10DCIS.com and MCF10CA1a – and compared the ability of the latter 3 lines to form tumors in immunodeficient mice. In addition, we also investigated expression of several key signaling proteins in the MCF10 cell series corresponding to different stages of breast cancer progression. MCF10DCIS.com and MCF10CA1a cells were highly tumorigenic; MCF10CA1a cells showed more aggressive tumor growth than MCF10DCIS.com cells. HRAS-driven cancer initiation stage was accompanied by the increased expression of c-Myc, cyclin D1 and IGF-IR. Tumorigenic cell lines expressed higher levels of pErk, pAkt, Stat3 and Pak4 compared to nontumorigenic cells. The expression of CD44v, CD44v3, CD44v6, ERBB2, Cox2 and Smad4 correlated with the increased tumorigenicity of the MCF10 cell lines. The differences in expression of signaling proteins involved in breast cancer progression may provide new insight into the mechanisms of tumorigenesis and useful information for development of targeted therapeutics.
机译：正常0否否否EN-US X-NONE X-NONE / *样式定义* / table.MsoNormalTable {mso-style-name：“ Table Normal”; mso-tstyle-rowband-size：0; mso-tstyle-colband-size：0; mso-style-noshow：是; mso-style-priority：99; mso-style-parent：“”; mso-padding-alt：0in 5.4pt 0in 5.4pt; mso-para-margin：0in; mso-para-margin-bottom：.0001pt; mso分页：寡妇孤儿;字体大小：10.0pt;乳腺癌是一种异质性疾病，通过多步过程发展，其分子基础仍然知之甚少。使用MCF10模型已经广泛研究了乳腺癌进展的分子机制。我们总结了有关MCF10细胞系列（MCF10A，MCF10AT1，MCF10DCIS.com和MCF10CA1a）中蛋白质差异表达的最新结果，并比较了后3个系在免疫缺陷小鼠中形成肿瘤的能力。此外，我们还研究了MCF10细胞系列中与乳腺癌进展不同阶段相对应的几种关键信号蛋白的表达。 MCF10DCIS.com和MCF10CA1a细胞具有高度致瘤性; MCF10CA1a细胞比MCF10DCIS.com细胞显示出更具侵略性的肿瘤生长。 HRAS驱动的癌症起始阶段伴随c-Myc，细胞周期蛋白D1和IGF-1R的表达增加。与非致瘤细胞相比，致瘤细胞系表达更高水平的pErk，pAkt，Stat3和Pak4。 CD44v，CD44v3，CD44v6，ERBB2，Cox2和Smad4的表达与MCF10细胞系致瘤性增加有关。参与乳腺癌进展的信号蛋白表达差异可能为肿瘤发生机理提供新见识，并为开发靶向治疗药物提供有用信息。

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