ArticleBMC systems biology2014
A bioinformatics approach reveals novel interactions of the OVOL transcription factors in the regulation of epithelial - mesenchymal cell reprogramming and cancer progression.
Article in BMC systems biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Article
- Single-cell resolution of MET- and EMT-like programs in osteoblasts during zebrafish fin regeneration.iScience · 2022Article
- Shavenbaby and Yorkie mediate Hippo signaling to protect adult stem cells from apoptosis.Nature communications · 2018Article
- Cellular responses to human cytomegalovirus infection: Induction of a mesenchymal-to-epithelial transition (MET) phenotype.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Discovery and validation of information theory-based transcription factor and cofactor binding site motifs.Nucleic acids research · 2017Article
- Article
- Expression of Ovol2 is related to epithelial characteristics and shows a favorable clinical outcome in hepatocellular carcinoma.OncoTargets and therapy · 2016Article
- Article
- OVOL guides the epithelial-hybrid-mesenchymal transition.Oncotarget · 2015Article
- Implications of the Hybrid Epithelial/Mesenchymal Phenotype in Metastasis.Frontiers in oncology · 2015Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundMesenchymal to Epithelial Transition (MET) plasticity is critical to cancer progression, and we recently showed that the OVOL transcription factors (TFs) are critical regulators of MET. Results of that work also posed the hypothesis that the OVOLs impact MET in a range of cancers. We now test this hypothesis by developing a model, OVOL Induced MET (OI-MET), and sub-model (OI-MET-TF), to characterize differential gene expression in MET common to prostate cancer (PC) and breast cancer (BC).
resultsIn the OI-MET model, we identified 739 genes differentially expressed in both the PC and BC models. For this gene set, we found significant enrichment of annotation for BC, PC, cancer, and MET, as well as regulation of gene expression by AP1, STAT1, STAT3, and NFKB1. Focusing on the target genes for these four TFs plus the OVOLs, we produced the OI-MET-TF sub-model, which shows even greater enrichment for these annotations, plus significant evidence of cooperation among these five TFs. Based on known gene/drug interactions, we prioritized targets in the OI-MET-TF network for follow-on analysis, emphasizing the clinical relevance of this work. Reflecting these results back to the OI-MET model, we found that binding motifs for the TF pair AP1/MYC are more frequent than expected and that the AP1/MYC pair is significantly enriched in binding in cancer models, relative to non-cancer models, in these promoters. This effect is seen in both MET models (solid tumors) and in non-MET models (leukemia). These results are consistent with our hypothesis that the OVOLs impact cancer susceptibility by regulating MET, and extend the hypothesis to include mechanisms not specific to MET.
conclusionsWe find significant evidence of the OVOL, AP1, STAT1, STAT3, and NFKB1 TFs having important roles in MET, and more broadly in cancer. We prioritize known gene/drug targets for follow-up in the clinic, and we show that the AP1/MYC TF pair is a strong candidate for intervention.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.