Journal
CANCER CELL
Volume 34, Issue 3, Pages 466-+Publisher
CELL PRESS
DOI: 10.1016/j.ccell.2018.08.001
Keywords
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Categories
Funding
- Cancer Center Core grant [CA014195]
- NIH/NCI [R35 CA197687]
- Susan G. Komen Foundation [SAC110036]
- BCRF
- [CA174430]
- [GM007752]
- [CA206416]
- [CA186043]
- [CA197699]
- NATIONAL CANCER INSTITUTE [F32CA174430, R01CA186043, F31CA206416, P30CA014195, R35CA197687, R35CA197699] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [T32GM007752] Funding Source: NIH RePORTER
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Cell state reprogramming during tumor progression complicates accurate diagnosis, compromises therapeutic effectiveness, and fuels metastatic dissemination. We used chromatin accessibility assays and transcriptional profiling during mammary development as an agnostic approach to identify factors that mediate cancer cell state interconversions. We show that fetal and adult basal cells share epigenetic features consistent with multi-lineage differentiation potential. We find that DNA-binding motifs for SOX transcription factors are enriched in chromatin that is accessible in stem/progenitor cells and inaccessible in differentiated cells. In both mouse and human tumors, SOX10 expression correlates with stem/progenitor identity, dedifferentiation, and invasive characteristics. Strikingly, we demonstrate that SOX10 binds to genes that regulate neural crest cell identity, and that SOX10-positive tumor cells exhibit neural crest cell features.
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