ChIP-seq analysis of genome-wide DNA-binding by STAT3 alternative spliceforms following Oncostatin M stimulation
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ABSTRACT:
PROVIDER: PRJNA527977 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR8750180.fastq.gz | Fastqsanger.gz | |||
| SRR8750173.fastq.gz | Fastqsanger.gz | |||
| SRR8750174.fastq.gz | Fastqsanger.gz | |||
| SRR8750176.fastq.gz | Fastqsanger.gz |
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Project description:Alternative splicing in the Signal Transducer and Activator of Transcription 3 (STAT3) transcription factor gene generates the STAT3α and STAT3β spliceforms that have identical DNA-binding domains but C-terminal transactivation domains that differ in both length and sequence. To delineate the impact that the different STAT3α and STAT3β transactivation domains have on cytokine-activated genome-wide DNA-binding, we measured STAT3α and STAT3β DNA-binding at identified STAT3 transcription factor binding sites within the mouse genome using cells engineered to express either the STAT3α or STAT3β spliceform only. The analyses show that ~40% of STAT3-bound genomic regions (2280 of 5343 regions) are commonly targeted by both STAT3 spliceforms. The remaining STAT3-bound genomic regions are preferentially targeted by either STAT3α or STAT3β (1450 and 1613 regions, respectively) and associated with genes enriched in unique biological functions. Motif enrichment analyses not only confirm the targeting of the canonical STAT3 target DNA motif by both spliceforms but reveal several co-occurring DNA motifs known to be targeted by transcription factors that can act cooperatively with STAT3 during target gene transcription regulation. Multiple additional co-occurring DNA motifs selectively enriched in STAT3α- or STAT3β-associated regions were also identified.
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Project description:Increasing evidence supports the idea that cancer cell plasticity promotes metastasis and tumor recurrence, resulting in patient mortality. While it is clear that the tumor microenvironment (TME) contributes to cancer cell plasticity, the specific TME factors most actively controlling plasticity remain largely unknown. Here, we performed a screen to identify TME cytokines and growth factors that promote epithelial-mesenchymal plasticity, and acquisition of cancer stem-cell (CSC) properties. Of 28 TME cytokines and growth factors tested, we identified Oncostatin M (OSM) as the most potent inducer of mesenchymal/CSC properties. OSM-induced plasticity was Signal Transducer and Activator of Transcription 3 (STAT3)-dependent, and also required a novel intersection with Transforming Growth Factor-β (TGF-β)/SMAD signaling. OSM/STAT3 activation promoted SMAD3 nuclear accumulation, DNA-binding, and induced SMAD3-dependent transcriptional activity. Suppression of TGF-β receptor activity or ablation of SMAD3 or SMAD4, but not SMAD2, strongly suppressed OSM/STAT3-mediated plasticity. Moreover, removal of OSM or inhibition of STAT3 or SMAD3 resulted in a marked reversion to a non-invasive, epithelial phenotype. We propose that, targeted blockade of the STAT3/SMAD3 axis in tumor cells may represent a novel therapeutic approach to prevent the plasticity required for metastatic progression and tumor recurrence.
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Project description:Oncostatin M (OSM) is an IL-6 family cytokine that is necessary for neutrophil recruitment in pneumonia by inducing STAT3-dependent production of CXCL5. We used microarrays to identify additional pathways affected by OSM neutralization in the lungs during pneumonia.
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Project description:The latent transcription factor STAT3 is a point of convergence for numerous oncogenic signaling pathways and is excessively activated in the majority of human epithelial cancers. STAT3 promotes many hallmarks of cancer including enhanced proliferation, increased survival, sustained angiogenesis, immune evasion and tumor-promoting inflammation. We performed chromatin immunoprecipitations (ChIP) followed by next-generation sequencing (ChIP-Seq) to identify genomic Stat3 binding sites in established gastric tumors of gp130F/F mutant mice (Tebbutt et al., 2002) following administration of recombinant human interleukin (IL)-6 or IL11. The study was designed to assess differences in Stat3 recruitment in response to IL6 and IL11, two cytokines which both activate Stat3 through the shared IL6 cytokine family receptor subunit gp130. In gp130F/F mice, a robust model for inflammation-associated intestinal-type gastric tumorigenesis, the Y757F knock-in mutation in the gp130 receptor triggers spontaneous gastric tumor formation in a strictly IL11-dependent manner, but independent of IL6 signaling (Ernst et al., 2008). Therefore, the study aimed to identify IL6- and IL11-specific Stat3 target genes. In total, we identified 948 or 961 significant Stat3-DNA interactions in gp130F/F tumors following IL6 or IL11 administration, respectively. These interactions were validated by binding motif analysis which showed that at least 30% of all Stat3-associated genomic regions comprise a Stat3 consensus binding sequence.
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