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Transgelin Silencing Induces Different Processes in Different Breast Cancer Cell Lines.
Proteomics ( IF 3.4 ) Pub Date : 2020-03-04 , DOI: 10.1002/pmic.201900383
Monika Dvorakova 1, 2 , Petr Lapcik 1 , Pavla Bouchalova 1 , Pavel Bouchal 1
Affiliation  

Transgelin is a protein reported to be a marker of several cancers. However, previous studies have shown both up- and down-regulation of transgelin in tumors when compared with non-tumor tissues and the mechanisms whereby transgelin may affect the development of cancer remain largely unknown. Transgelin is especially abundant in smooth muscle cells and is associated with actin stress fibers. These contractile structures participate in cell motility, adhesion, and the maintenance of cell morphology. Here, the role of transgelin in breast cancer is focused on. Initially, the effects of transgelin on cell migration of the breast cancer cell lines, BT 549 and PMC 42, is studied. Interestingly, transgelin silencing increased the migration of PMC 42 cells, but decreased the migration of BT 549 cells. To clarify these contradictory results, the changes in protein abundances after transgelin silencing in these two cell lines are analyzed using quantitative proteomics. The results confirmed the role of transgelin in the migration of BT 549 cells and suggest the involvement of transgelin in apoptosis and small molecule biochemistry in PMC 42 cells. The context-dependent function of transgelin reflects the different molecular backgrounds of these cell lines, which differ in karyotypes, mutation statuses, and proteome profiles.

中文翻译:

Transgelin沉默在不同的乳腺癌细胞系中诱导不同的过程。

Transgelin是一种蛋白质,据报道是几种癌症的标志物。但是,先前的研究表明,与非肿瘤组织相比,肿瘤中转胶蛋白的上调和下调均不明确,而转胶蛋白可能影响癌症发展的机制仍然未知。Transgelin在平滑肌细胞中尤其丰富,并与肌动蛋白应激纤维有关。这些收缩结构参与细胞运动,粘附和细胞形态的维持。在这里,着重介绍了转胶蛋白在乳腺癌中的作用。最初,研究了转蛋白对乳腺癌细胞系BT 549和PMC 42的细胞迁移的影响。有趣的是,转胶蛋白沉默增加了PMC 42细胞的迁移,但降低了BT 549细胞的迁移。为了澄清这些矛盾的结果,使用定量蛋白质组学分析了这两种细胞中转胶蛋白沉默后蛋白质丰度的变化。结果证实了转凝蛋白在BT 549细胞迁移中的作用,并暗示了转凝蛋白与PMC 42细胞的凋亡和小分子生物化学有关。Transgelin的上下文相关功能反映了这些细胞系的不同分子背景,这些背景在核型,突变状态和蛋白质组谱方面均不同。
更新日期:2020-04-22
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