Battilana Giusy, Zanconato Francesca, Piccolo Stefano
Department of Molecular Medicine, University of Padua, Via G. Colombo 3, 35131, Padua, Italy.
IFOM, the FIRC Institute of Molecular Oncology, Milan, Italy.
Cell Stress. 2021 Oct 29;5(11):167-172. doi: 10.15698/cst2021.11.258. eCollection 2021 Nov.
Dysregulated gene expression is intrinsic to cell transformation, tumorigenesis and metastasis. Cancer-specific gene-expression profiles stem from gene regulatory networks fueled by genetic and epigenetic defects, and by abnormal signals of the tumor microenvironment. These oncogenic signals ultimately engage the transcriptional machinery on the cis -regulatory elements of a host of effector genes, through recruitment of transcription factors (TFs), co-activators and chromatin regulators. That said, whether gene-expression in cancer cells is the chaotic product of myriad regulations or rather a relatively ordered process orchestrated by few TFs (master regulators) has long remained enigmatic. Recent work on the YAP/TAZ co-activators has been instrumental to break new ground into this outstanding issue, revealing that tumor cells hijack growth programs that are active during development and regeneration through engagement of a small set of interconnected TFs and their nuclear partners.
基因表达失调是细胞转化、肿瘤发生和转移的内在特征。癌症特异性基因表达谱源于由遗传和表观遗传缺陷以及肿瘤微环境的异常信号驱动的基因调控网络。这些致癌信号最终通过招募转录因子（TFs）、共激活因子和染色质调节因子，与众多效应基因的顺式调控元件上的转录机制相互作用。也就是说，癌细胞中的基因表达是无数调控的混乱产物，还是由少数TFs（主调控因子）精心编排的相对有序的过程，长期以来一直是个谜。最近关于YAP/TAZ共激活因子的研究有助于在这个突出问题上开辟新的领域，揭示肿瘤细胞通过一小部分相互连接的TFs及其核伴侣的参与，劫持了在发育和再生过程中活跃的生长程序。
