ArticleBiochemical and biophysical research communications2015
Identification of a PEAK1/ZEB1 signaling axis during TGFβ/fibronectin-induced EMT in breast cancer.
Article in Biochemical and biophysical research communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Is overexpression of TWIST, a transcriptional factor, a prognostic biomarker of head and neck carcinoma? Evidence from fifteen studies.Scientific reports · 2015Pooled it
- PEAK1 promotes prostate cancer progression and docetaxel resistance by mediating the polarization of tumor-associated macrophages.European journal of medical research · 2026Article
- Toll-Like receptor 3-mediated interferon-β production is suppressed by oncostatin m and a broader epithelial-mesenchymal transition program.Breast cancer research : BCR · 2024Article
- Role of anoikis-related gene RAC3 in prognosis, immune microenvironment, and contribution to malignant behaviorFrontiers in pharmacology · 2024Article
- Preneoplastic stromal cells promote BRCA1-mediated breast tumorigenesis.Nature genetics · 2023Article
- Dual inhibition of TGF-β and PD-L1: a novel approach to cancer treatment.Molecular oncology · 2022Review
- Pseudopodium enriched atypical kinase 1(PEAK1) promotes invasion and of melanoma cells by activating JAK/STAT3 signals.Bioengineered · 2021Article
- Article
- ZEB1-Mediated Transcriptional Upregulation of circWWC3 Promotes Breast Cancer Progression through Activating Ras Signaling Pathway.Molecular therapy. Nucleic acids · 2020Article
- Phospho-PTM proteomic discovery of novel EPO- modulated kinases and phosphatases, including PTPN18 as a positive regulator of EPOR/JAK2 Signaling.Cellular signalling · 2020Article
- Comprehensive Proteomic Characterization Reveals Subclass-Specific Molecular Aberrations within Triple-negative Breast Cancer.iScience · 2020Article
- WD Repeat Domain 5 Promotes Invasion, Metastasis and Tumor Growth in Glioma Through Up-Regulated Zinc Finger E-Box Binding Homeobox 1 Expression.Cancer management and research · 2020Article
- DHPS-dependent hypusination of eIF5A1/2 is necessary for TGFβ/fibronectin-induced breast cancer metastasis and associates with prognostically unfavorable genomic alterations in TP53.Biochemical and biophysical research communications · 2019Article
- EMT-related protein expression in polyploid giant cancer cells and their daughter cells with different passages after triptolide treatment.Medical oncology (Northwood, London, England) · 2019Article
- Review
- Article
- SHEDding light on the role of Pragmin pseudo-kinases in cancer.American journal of cancer research · 2019Article
- Loss of miR-144 signaling interrupts extracellular matrix remodeling after myocardial infarction leading to worsened cardiac function.Scientific reports · 2018Article
- Identification of biomarkers associated with partial epithelial to mesenchymal transition in the secretome of slug over-expressing hepatocellular carcinoma cells.Cellular oncology (Dordrecht, Netherlands) · 2018Article
- Overexpression of PEAK1 contributes to epithelial-mesenchymal transition and tumor metastasis in lung cancer through modulating ERK1/2 and JAK2 signaling.Cell death & disease · 2018Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Transforming Growth Factor beta (TGFβ) is the archetypal member of the TGFβ superfamily of ligands and has pleiotropic functions during normal development, adult tissue homeostasis and pathophysiological processes such as cancer. In epithelial cancers TGFβ signaling can either suppress tumor growth or promote metastasis via the induction of a well-characterized epithelial-mesenchymal transition (EMT) program. We recently reported that PEAK1 kinase mediates signaling cross talk between TGFβ receptors and integrin/Src/MAPK pathways and functions as a critical molecular regulator of TGFβ-induced breast cancer cell proliferation, migration, EMT and metastasis. Here, we examined the breast cancer cell contexts in which TGFβ induces both EMT and PEAK1, and discovered this event to be unique to oncogene-transformed mammary epithelial cells and triple-negative breast cancer cells. Using the Cancer BioPortal database, we identified PEAK1 co-expressors across multiple malignancies that are also common to the TGFβ response gene signature (TBRS). We then used the ScanSite database to identify predicted protein-protein binding partners of PEAK1 and the PEAK1-TBRS co-expressors. Analysis of the Cytoscape interactome and Babelomics-derived gene ontologies for a novel gene set including PEAK1, CRK, ZEB1, IL11 and COL4A1 enabled us to hypothesize that PEAK1 may be regulating TGFβ-induced EMT via its interaction with or regulation of these other genes. In this regard, we have demonstrated that PEAK1 is necessary for TGFβ to induce ZEB1-mediated EMT in the context of fibronectin/ITGB3 activation. These studies and future mechanistic studies will pave the way toward identifying the context in which TGFβ blockade may significantly improve breast cancer patient outcomes.
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