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| Status |
Public on Oct 07, 2022 |
| Title |
MLL3 Loss Drives Metastasis by Promoting a Hybrid Epithelial-Mesenchymal Transition State [ChIP-seq histone marker] |
| Organism |
Homo sapiens |
| Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
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| Summary |
Phenotypic plasticity associated with the hybrid epithelial-mesenchymal transition (EMT) state is crucial to metastatic seeding and outgrowth. However, the mechanisms controlling the induction of hybrid EMT remain poorly defined.
We showed that deletion of the epigenetic regulator MLL3, a tumor suppressor frequently altered in human cancer, promoted the acquisition of the hybrid EMT state in both epithelial and mesenchymal breast cancer cells by facilitating EMT and MET, distinct from other known EMT regulators mediating unidirectional changes. Consequently, MLL3 deletion greatly increased metastasis by enhancing metastatic outgrowth during colonization. Mechanistically, MLL3 loss led to IFNγ signaling upregulation, which contributes to the induction of hybrid EMT cells and the enhanced metastatic capacity.
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| Overall design |
Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for H3K27ac, H3K4me1 and H3K4me3 in MLL3-WT and Mut MDA-MB-231 cells.
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| Contributor(s) |
Cui J, Zhang C, Guo W |
| Citation(s) |
36604594 |
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| Submission date |
Jun 22, 2022 |
| Last update date |
Jan 07, 2023 |
| Contact name |
Jihong Cui |
| E-mail(s) |
jihong.cui@einsteinmed.edu
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| Phone |
7186781277
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| Organization name |
Albert einstein college of medicine
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| Lab |
Wenjun Guo
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| Street address |
1301 Morris Park Avenue, Room 108/114
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| City |
Bronx |
| State/province |
NY |
| ZIP/Postal code |
10461 |
| Country |
USA |
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| Platforms (1) |
| GPL20301 |
Illumina HiSeq 4000 (Homo sapiens) |
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| Samples (16)
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| GSM6260171 |
MDA-MB-231 sgNT1, input, biological replicate1 |
| GSM6260172 |
MDA-MB-231 sgNT1, input, biological replicate2 |
| GSM6260173 |
MDA-MB-231 sgNT1, H3K4me1, biological replicate1 |
| GSM6260174 |
MDA-MB-231 sgNT1, H3K4me1, biological replicate2 |
| GSM6260175 |
MDA-MB-231 sgNT1, H3K4me3, biological replicate1 |
| GSM6260176 |
MDA-MB-231 sgNT1, H3K4me3, biological replicate2 |
| GSM6260177 |
MDA-MB-231 sgNT1, H3K27ac, biological replicate1 |
| GSM6260178 |
MDA-MB-231 sgNT1, H3K27ac, biological replicate2 |
| GSM6260179 |
MDA-MB-231 sgMLL3, input, biological replicate1 |
| GSM6260180 |
MDA-MB-231 sgMLL3, input, biological replicate2 |
| GSM6260181 |
MDA-MB-231 sgMLL3, H3K4me1, biological replicate1 |
| GSM6260182 |
MDA-MB-231 sgMLL3, H3K4me1, biological replicate2 |
| GSM6260183 |
MDA-MB-231 sgMLL3, H3K4me3, biological replicate1 |
| GSM6260184 |
MDA-MB-231 sgMLL3, H3K4me3, biological replicate2 |
| GSM6260185 |
MDA-MB-231 sgMLL3, H3K27ac, biological replicate1 |
| GSM6260186 |
MDA-MB-231 sgMLL3, H3K27ac, biological replicate2 |
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| This SubSeries is part of SuperSeries: |
| GSE171447 |
MLL3 loss drives metastasis and therapeutic resistance by promoting a hybrid EMT state |
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| Relations |
| BioProject |
PRJNA851731 |
| Supplementary file |
Size |
Download |
File type/resource |
| GSE206656_RAW.tar |
6.2 Gb |
(http)(custom) |
TAR (of BW) |
SRA Run Selector |
| Raw data are available in SRA |
| Processed data provided as supplementary file |
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