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首页> 外文期刊>Journal of Clinical Medicine >Multi-Omics Characterization of the Spontaneous Mesenchymal–Epithelial Transition in the PMC42 Breast Cancer Cell Lines
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Multi-Omics Characterization of the Spontaneous Mesenchymal–Epithelial Transition in the PMC42 Breast Cancer Cell Lines

机译：PMC42乳腺癌细胞系自发间质-上皮转化的多组学特征

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Epithelial–mesenchymal plasticity (EMP), encompassing epithelial–mesenchymal transition (EMT) and mesenchymal–epithelial transition (MET), are considered critical events for cancer metastasis. We investigated chromosomal heterogeneity and chromosomal instability (CIN) profiles of two sister PMC42 breast cancer (BC) cell lines to assess the relationship between their karyotypes and EMP phenotypic plasticity. Karyotyping by GTG banding and exome sequencing were aligned with SWATH quantitative proteomics and existing RNA-sequencing data from the two PMC42 cell lines; the mesenchymal, parental PMC42-ET cell line and the spontaneously epithelially shifted PMC42-LA daughter cell line. These morphologically distinct PMC42 cell lines were also compared with five other BC cell lines (MDA-MB-231, SUM-159, T47D, MCF-7 and MDA-MB-468) for their expression of EMP and cell surface markers, and stemness and metabolic profiles. The findings suggest that the epithelially shifted cell line has a significantly altered ploidy of chromosomes 3 and 13, which is reflected in their transcriptomic and proteomic expression profiles. Loss of the TGFβR2 gene from chromosome 3 in the epithelial daughter cell line inhibits its EMT induction by TGF-β stimulus. Thus, integrative ‘omics’ characterization established that the PMC42 system is a relevant MET model and provides insights into the regulation of phenotypic plasticity in breast cancer.
机译：上皮-间质可塑性（EMP），包括上皮-间质转化（EMT）和间质-上皮转化（MET），被认为是癌症转移的关键事件。我们调查了两个姐妹PMC42乳腺癌（BC）细胞系的染色体异质性和染色体不稳定性（CIN）谱，以评估它们的核型与EMP表型可塑性之间的关系。通过GTG带和外显子组测序进行的核型分析与SWATH定量蛋白质组学和来自两个PMC42细胞系的现有RNA测序数据进行了比对。间充质亲代PMC42-ET细胞系和自发上皮转移的PMC42-LA子代细胞系。还比较了这些形态上不同的PMC42细胞系与其他五种BC细胞系（MDA-MB-231，SUM-159，T47D，MCF-7和MDA-MB-468）的EMP表达和细胞表面标记以及干性和代谢状况。这些发现表明，上皮转移的细胞系具有明显改变的3号和13号染色体倍性，这反映在它们的转录组和蛋白质组表达谱中。上皮子细胞系中第3号染色体的TGFβR2基因缺失，抑制了TGF-β刺激的EMT诱导。因此，综合的“组学”特征确定了PMC42系统是一种相关的MET模型，并提供了对乳腺癌表型可塑性调节的见解。

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