Etiology of super-enhancer reprogramming and activation in cancer.
Etiology of super-enhancer reprogramming and activation in cancer.
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DOI：
10.1186/s13072-023-00502-w
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发表时间：
2023-07-06
影响因子：
3.9
通讯作者：
中科院分区：
文献类型：
--
作者：
超级增强子是大的，密集集中的增强子带，调节对细胞身份至关重要的基因。肿瘤发生伴随着超级增强子景观的变化。这些异常的超级增强子通常形成以激活原癌基因或癌细胞所依赖的其他基因，其引发肿瘤发生，促进肿瘤增殖，并增加癌细胞在肿瘤微环境中存活的适应性。这些包括公认的癌症背景下增殖的主要调节因子，例如转录因子MYC，与正常组织相比，其处于癌症中获得的众多超级增强子的控制下。本综述将涵盖癌症中这些超级增强子变化的细胞内在和细胞外在病因学，包括体细胞突变，拷贝数变异，融合事件，染色体外DNA和3D染色质结构，以及炎症，细胞外信号传导和肿瘤微环境激活的那些。
Super-enhancers are large, densely concentrated swaths of enhancers that regulate genes critical for cell identity. Tumorigenesis is accompanied by changes in the super-enhancer landscape. These aberrant super-enhancers commonly form to activate proto-oncogenes, or other genes upon which cancer cells depend, that initiate tumorigenesis, promote tumor proliferation, and increase the fitness of cancer cells to survive in the tumor microenvironment. These include well-recognized master regulators of proliferation in the setting of cancer, such as the transcription factor MYC which is under the control of numerous super-enhancers gained in cancer compared to normal tissues. This Review will cover the expanding cell-intrinsic and cell-extrinsic etiology of these super-enhancer changes in cancer, including somatic mutations, copy number variation, fusion events, extrachromosomal DNA, and 3D chromatin architecture, as well as those activated by inflammation, extra-cellular signaling, and the tumor microenvironment.
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影响因子：
50.3
作者：
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Dalla-Favera R
YAP的相位分离重新组织了基因组拓扑，以进行长期YAP靶基因表达。
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64.8
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Ahn JH;Davis ES;Daugird TA;Zhao S;Quiroga IY;Uryu H;Li J;Storey AJ;Tsai YH;Keeley DP;Mackintosh SG;Edmondson RD;Byrum SD;Cai L;Tackett AJ;Zheng D;Legant WR;Phanstiel DH;Wang GG
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Wang GG
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50.3
作者：
Bai, Longchuan;Zhou, Haibin;Wang, Shaomeng
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Wang, Shaomeng
弥漫性大 B 细胞淋巴瘤中超级增强子相关依赖性的发现和表征。
影响因子：
50.3
作者：
Chapuy B;McKeown MR;Lin CY;Monti S;Roemer MG;Qi J;Rahl PB;Sun HH;Yeda KT;Doench JG;Reichert E;Kung AL;Rodig SJ;Young RA;Shipp MA;Bradner JE
通讯作者：
Bradner JE