生物
癌变
癌症研究
基因表达
胚胎干细胞
谱系(遗传)
生物发生
癌基因
基因表达调控
基因
细胞生物学
遗传学
细胞周期
作者
Delaney K. Sullivan,Anja Deutzmann,Josiah Yarbrough,Maya S. Krishnan,Arvin M. Gouw,David I. Bellovin,Stacey J. Adam,Daniel F. Liefwalker,Renumathy Dhanasekaran,Dean W. Felsher
出处
期刊:Oncogene
[Springer Nature]
日期:2022-10-07
卷期号:41 (45): 4960-4970
被引量:7
标识
DOI:10.1038/s41388-022-02458-9
摘要
MYC is a transcription factor frequently overexpressed in cancer. To determine how MYC drives the neoplastic phenotype, we performed transcriptomic analysis using a panel of MYC-driven autochthonous transgenic mouse models. We found that MYC elicited gene expression changes mostly in a tissue- and lineage-specific manner across B-cell lymphoma, T-cell acute lymphoblastic lymphoma, hepatocellular carcinoma, renal cell carcinoma, and lung adenocarcinoma. However, despite these gene expression changes being mostly tissue-specific, we uncovered a convergence on a common pattern of upregulation of embryonic stem cell gene programs and downregulation of tissue-of-origin gene programs across MYC-driven cancers. These changes are representative of lineage dedifferentiation, that may be facilitated by epigenetic alterations that occur during tumorigenesis. Moreover, while several cellular processes are represented among embryonic stem cell genes, ribosome biogenesis is most specifically associated with MYC expression in human primary cancers. Altogether, MYC’s capability to drive tumorigenesis in diverse tissue types appears to be related to its ability to both drive a core signature of embryonic genes that includes ribosomal biogenesis genes as well as promote tissue and lineage specific dedifferentiation.
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