Science for Life Laboratory, Royal Institute of Technology (KTH), SE-17121 Solna, Sweden.
Proc Natl Acad Sci U S A. 2013 Apr 23;110(17):6853-8. doi: 10.1073/pnas.1216436110. Epub 2013 Apr 8.
The transformation of normal cells to malignant, metastatic tumor cells is a multistep process caused by the sequential acquirement of genetic changes. To identify these changes, we compared the transcriptomes and levels and distribution of proteins in a four-stage cell model of isogenically matched normal, immortalized, transformed, and metastatic human cells, using deep transcriptome sequencing and immunofluorescence microscopy. The data show that ∼6% (n = 1,357) of the human protein-coding genes are differentially expressed across the stages in the model. Interestingly, the majority of these genes are down-regulated, linking malignant transformation to dedifferentiation. The up-regulated genes are mainly components that control cellular proliferation, whereas the down-regulated genes consist of proteins exposed on or secreted from the cell surface. As many of the identified gene products control basic cellular functions that are defective in cancers, the data provide candidates for follow-up studies to investigate their functional roles in tumor formation. When we further compared the expression levels of four of the identified proteins in clinical cancer cohorts, similar differences were observed between benign and cancer cells, as in the cell model. This shows that this comprehensive demonstration of the molecular changes underlying malignant transformation is a relevant model to study the process of tumor formation.
正常细胞向恶性、转移性肿瘤细胞的转化是一个多步骤的过程,是通过连续获得遗传变化引起的。为了识别这些变化,我们使用深度转录组测序和免疫荧光显微镜,比较了同源匹配的正常、永生化、转化和转移性人细胞的四阶段细胞模型中的转录组和蛋白质的水平和分布。数据显示,模型中约有 6%(n=1357)的人类蛋白质编码基因在不同阶段存在差异表达。有趣的是,这些基因中的大多数下调,将恶性转化与去分化联系起来。上调的基因主要是控制细胞增殖的成分,而下调的基因则包括暴露在细胞表面或从细胞表面分泌的蛋白质。由于所鉴定的基因产物中的许多都控制着癌症中存在缺陷的基本细胞功能,这些数据为后续研究提供了候选基因,以研究它们在肿瘤形成中的功能作用。当我们进一步比较在临床癌症队列中鉴定出的四种蛋白质的表达水平时,良性和癌细胞之间也观察到了类似的差异,与细胞模型中的情况一样。这表明,这种对恶性转化潜在分子变化的全面展示是研究肿瘤形成过程的一个相关模型。
Proc Natl Acad Sci U S A. 2013-4-8
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