Abstract：
:Liposarcomas (LPSs) are a group of malignant mesenchymal tumors showing adipocytic differentiation. Here, to gain insight into the enhancer dysregulation and transcriptional addiction in this disease, we chart super-enhancer structures in both LPS tissues and cell lines. We identify a bromodomain and extraterminal (BET) protein-cooperated FUS-DDIT3 function in myxoid LPS and a BET protein-dependent core transcriptional regulatory circuitry consisting of FOSL2, MYC, and RUNX1 in de-differentiated LPS. Additionally, SNAI2 is identified as a crucial downstream target that enforces both proliferative and metastatic potentials to de-differentiated LPS cells. Genetic depletion of BET genes, core transcriptional factors, or SNAI2 mitigates consistently LPS malignancy. We also reveal a compelling susceptibility of LPS cells to BET protein degrader ARV-825. BET protein depletion confers additional advantages to circumvent acquired resistance to Trabectedin, a chemotherapy drug for LPS. Moreover, this study provides a framework for discovering and targeting of core oncogenic transcriptional programs in human cancers.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Chen Y,Xu L,Mayakonda A,Huang ML,Kanojia D,Tan TZ,Dakle P,Lin RY,Ke XY,Said JW,Chen J,Gery S,Ding LW,Jiang YY,Pang A,Puhaindran ME,Goh BC,Koeffler HPdoi
10.1038/s41467-019-09257-zsubject
Has Abstractpub_date
2019-03-22 00:00:00pages
1353issue
1issn
2041-1723pii
10.1038/s41467-019-09257-zjournal_volume
10pub_type
杂志文章abstract：:Breast cancer metastasis involves lymphatic dissemination in addition to hematogenous spreading. Although stromal lymphatic vessels (LVs) serve as initial metastatic routes, roles of organ-residing LVs are underinvestigated. Here we show that lymphatic endothelial cells (LECs), a component of LVs within pre-metastatic...
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