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首页> 外文期刊>Cell and Tissue Research >Tamoxifen-resistant, ER-positive MAC 51 cell line with a high metastatic potential developed from a spontaneous breast cancer mouse model.
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Tamoxifen-resistant, ER-positive MAC 51 cell line with a high metastatic potential developed from a spontaneous breast cancer mouse model.

机译：从自发性乳腺癌小鼠模型发展出具有高转移潜力的抗他莫昔芬，ER阳性的MAC 51细胞系。

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We developed and characterized an estrogen-responsive and ER-positive murine breast cancer cell line (MAC51) from a spontaneous breast cancer animal model. These cells are overexpressed with K8, K18 and K19 proteins in an immunofluoresence assay. Upregulation of ER alpha was observed in the immunofluoresence assay, real-time PCR analysis and western blot assay. A colocalization experiment in MAC 51 showed cytoplasmic colocalization of K18 and K19 proteins with ER α. Real-time analysis of tumor samples from engrafted animals, MAC 51, metastatic liver and metastatic ovary revealed overexpression of K8 and K18 compared to the respective controls. A hormone responsive experiment in immunodeficient mice showed highly significant decreases in estrogen and tumor volume after 14 days ovariectomization. The tumorogenicity assay showed higher (3?×?10 (5)) and lower (3?×?10(4)) concentrations of MAC 51 cells that developed tumors within 2?weeks post-transplantation. Tumor morphology and histology resembled a sarcoma pattern but our spontaneous model appeared in an adenocarcinoma pattern. Metastasis to different organs occurred through hematogenous and lymphatic routes. We assessed the potency of the anticancer effect in MAC 51 cells by treating various anticancer drugs with E2, followed by studying apoptotic gene expression profiles. E2 and E2+ tamoxifen-treated cells showed upregulation of apoptotic genes caspase 1, 3, 9, P53 and Bcl-xl but the tamoxifen- and paclitaxel-treated cells did not upregulate the apoptotic genes. Tamoxifen-resistant, ER-positive and high metastatic potential cell lines from murine origin are very rare. Also, estrogen greatly induced apoptosis in this cell line, hence MAC 51 has a greater application potential to evaluate low doses of estrogen with other targeted therapeutic drugs to treat breast cancer.
机译：我们从自然乳腺癌动物模型中开发并鉴定了雌激素反应性和ER阳性小鼠乳腺癌细胞系（MAC51）。在免疫荧光测定中，这些细胞用K8，K18和K19蛋白过度表达。在免疫荧光测定，实时PCR分析和蛋白质印迹测定中观察到ERα的上调。在MAC 51中进行的共定位实验显示，K18和K19蛋白与ERα在细胞质中共定位。对来自移植动物，MAC 51，转移性肝和转移性卵巢的肿瘤样品的实时分析显示，与各自的对照相比，K8和K18的过表达。在免疫缺陷小鼠中进行的激素反应性实验显示，去卵巢14天后雌激素和肿瘤体积显着降低。致瘤性分析显示，在移植后2周内出现肿瘤的MAC 51细胞浓度较高（3？×？10（5））和较低（3？×？10（4））。肿瘤的形态学和组织学类似肉瘤模式，但我们的自发模型以腺癌模式出现。通过血行和淋巴途径转移到不同器官。我们通过用E2处理各种抗癌药物，然后研究凋亡基因的表达谱，评估了MAC 51细胞中抗癌作用的效力。 E2和E2 +他莫昔芬处理的细胞显示凋亡基因caspase 1、3、9，P53和Bcl-xl上调，但他莫昔芬和紫杉醇处理的细胞没有上调凋亡基因。来自鼠源的抗他莫昔芬，ER阳性和高转移潜能的细胞系非常罕见。而且，雌激素极大地诱导了该细胞系的凋亡，因此MAC 51具有更大的应用潜力，可与其他靶向治疗药物一起评估低剂量的雌激素来治疗乳腺癌。

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