CAS Key Laboratory of Genome Sciences and Information, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing 100029, China.
Genomics Proteomics Bioinformatics. 2012 Dec;10(6):326-35. doi: 10.1016/j.gpb.2012.11.001. Epub 2012 Dec 4.
Immortality and tumorigenicity are two distinct characteristics of cancers. Immortalization has been suggested to precede tumorigenesis. To understand the molecular mechanisms of tumorigenicity and cancer progression in mammary epithelium, we established a tumorigenic cell model by means of heavy-ion radiation of an immortal cell model, which was created by overexpressing the human telomerase reverse transcriptase (hTERT) in normal human mammary epithelial cells. We examined the expression profile of this tumorigenic cell line (T_hMEC) using the hTERT-overexpressing immortal cell line (I_hMEC) as a control. In-depth RNA-seq data was generated by using the next-generation sequencing (NGS) platform (Life Technologies SOLiD3). We found that house-keeping (HK) and tissue-specific (TS) genes were differentially regulated during the tumorigenic process. HK genes tended to be activated while TS genes tended to be repressed. In addition, the HK genes and TS genes tended to contribute differentially to the variation of gene expression at different RPKM (gene expression in reads per exon kilobase per million mapped sequence reads) levels. Based on transcriptome analysis of the two cell lines, we defined 7053 differentially-expressed genes (DEGs) between immortality and tumorigenicity. Differential expression of 20 manually-selected genes was further validated using qRT-PCR. Our observations may help to further our understanding of cellular mechanism(s) in the transition from immortalization to tumorigenesis.
永生性和致瘤性是癌症的两个截然不同的特征。人们认为永生性先于致瘤性发生。为了理解乳腺上皮细胞的致瘤性和癌症进展的分子机制,我们通过重离子辐射过表达人端粒酶逆转录酶(hTERT)的正常人类乳腺上皮细胞的永生细胞模型,建立了一个致瘤细胞模型。我们使用过表达 hTERT 的永生细胞系(I_hMEC)作为对照,检查了这种致瘤细胞系(T_hMEC)的表达谱。我们使用下一代测序(NGS)平台(Life Technologies SOLiD3)生成了深度 RNA-seq 数据。我们发现,在致瘤过程中,管家(HK)和组织特异性(TS)基因的表达存在差异调节。HK 基因倾向于激活,而 TS 基因倾向于被抑制。此外,HK 基因和 TS 基因在不同 RPKM(外显子每百万映射序列读数以每千碱基读取表达)水平上对基因表达变化的贡献也存在差异。基于这两种细胞系的转录组分析,我们定义了永生性和致瘤性之间的 7053 个差异表达基因(DEGs)。使用 qRT-PCR 进一步验证了 20 个手动选择基因的差异表达。我们的观察结果可能有助于进一步了解从永生性到致瘤性的细胞机制。