Nfib Promotes Metastasis through a Widespread Increase in Chromatin Accessibility

被引：292

作者：

Denny, Sarah K. ^{[1
]}

Yang, Dian ^{[2
]}

Chuang, Chen-Hua ^{[3
]}

Brady, Jennifer J. ^{[3
]}

Lim, Jing Shan ^{[2
]}

Gruner, Barbara M. ^{[3
]}

Chiou, Shin-Heng ^{[3
]}

Schep, Alicia N. ^{[3
]}

Baral, Jessika ^{[3
]}

Hamard, Cecile ^{[7
]}

Antoine, Martine ^{[7
]}

Wislez, Marie ^{[7
]}

Kong, Christina S. ^{[4
]}

Connolly, Andrew J. ^{[4
]}

Park, Kwon-Sik ^{[8
]}

Sage, Julien ^{[2
,3
,5
,6
]}

Greenleaf, William J. ^{[1
,3
,9
]}

Winslow, Monte M. ^{[2
,3
,4
,5
]}

机构：

[1] Stanford Univ, Sch Med, Biophys Program, Stanford, CA 94305 USA

[2] Stanford Univ, Sch Med, Canc Biol Program, Stanford, CA 94305 USA

[3] Stanford Univ, Dept Genet, Sch Med, Stanford, CA 94305 USA

[4] Stanford Univ, Dept Pathol, Sch Med, Stanford, CA 94305 USA

[5] Stanford Univ, Stanford Canc Inst, Sch Med, Stanford, CA 94305 USA

[6] Stanford Univ, Dept Pediat, Sch Med, Stanford, CA 94305 USA

[7] Univ Paris 06, Hop Tenon, APHP, Serv Pneumol, F-75020 Paris, France

[8] Univ Virginia, Sch Med, Dept Microbiol Immunol & Canc Biol, Charlottesville, VA 22908 USA

[9] Stanford Univ, Dept Appl Phys, Stanford, CA 94305 USA

来源：

CELL | 2016年 / 166卷 / 02期

关键词：

CELL LUNG-CANCER; TRANSCRIPTION FACTORS; NUCLEAR FACTOR-1; TUMOR-CELLS; GENE; DYNAMICS; ACTIVATION; MIGRATION; ONCOGENE; SURVIVAL;

D O I：

10.1016/j.cell.2016.05.052

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Metastases are the main cause of cancer deaths, but the mechanisms underlying metastatic progression remain poorly understood. We isolated pure populations of cancer cells from primary tumors and metastases from a genetically engineered mouse model of human small cell lung cancer ( SCLC) to investigate the mechanisms that drive the metastatic spread of this lethal cancer. Genome-wide characterization of chromatin accessibility revealed the opening of large numbers of distal regulatory elements across the genome during metastatic progression. These changes correlate with copy number amplification of the Nfib locus, and differentially accessible sites were highly enriched for Nfib transcription factor binding sites. Nfib is necessary and sufficient to increase chromatin accessibility at a large subset of the intergenic regions. Nfib promotes pro-metastatic neuronal gene expression programs and drives the metastatic ability of SCLC cells. The identification of widespread chromatin changes during SCLC progression reveals an unexpected global reprogramming during metastatic progression.

引用

页码：328 / 342

页数：15

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