Christopher R. Sutton

ORCID: 0000-0002-7881-8254
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About
Contact & Profiles
Research Areas
  • Cancer Cells and Metastasis
  • RNA modifications and cancer
  • Immune Cell Function and Interaction
  • Cancer-related molecular mechanisms research
  • Protein Tyrosine Phosphatases
  • T-cell and B-cell Immunology
  • Signaling Pathways in Disease
  • NF-κB Signaling Pathways
  • Epigenetics and DNA Methylation
  • Genomics and Chromatin Dynamics
  • CAR-T cell therapy research
  • Cell death mechanisms and regulation
  • Cytokine Signaling Pathways and Interactions
  • FOXO transcription factor regulation
  • Nutrition, Genetics, and Disease

University of Canberra
2016-2019

ACT Government
2016-2017

Applied Science Private University
2015

Complex regulatory networks control epithelial-to-mesenchymal transition (EMT) but the underlying epigenetic is poorly understood. Lysine-specific demethylase 1 (LSD1) a key histone that alters landscape. Here we explored role of LSD1 in global regulation EMT, cancer stem cells (CSCs), tumour microenvironment, and therapeutic resistance breast cancer. induced pan-genomic gene expression implicated EMT selectively elicits programs CSCs whilst repressing non-CSC programs. phosphorylation at...

10.1038/s41598-017-17913-x article EN cc-by Scientific Reports 2018-01-02

Dual-specificity phosphatases (DUSPs) dephosphorylate threonine/serine and tyrosine residues on their substrates. Here we show that DUSP1, DUSP4, DUSP6 are involved in epithelial-to-mesenchymal transition (EMT) breast cancer stem cell (CSC) regulation. induced during EMT a PKC pathway signal-mediated model. We for the first time key chromatin-associated kinase PKC-θ directly regulates subset of DUSP family members. globally but differentially co-exist with enhancer permissive active histone...

10.1371/journal.pone.0148065 article EN cc-by PLoS ONE 2016-02-09

Epithelial-to-mesenchymal transition (EMT) is physiological in embryogenesis and wound healing but also associated with the formation of cancer stem cells (CSCs). Many EMT signaling pathways are implicated CSC formation, precise underlying mechanisms remain elusive. We have previously demonstrated that PKC critical for induction inducible breast EMT/CSC models. Here, we used formaldehyde-assisted isolation regulatory elements-sequencing (FAIRE-seq) to investigate DNA accessibility changes...

10.1080/19491034.2016.1150392 article EN Nucleus 2016-03-01

DUSP6 is a dual-specificity phosphatase (DUSP) involved in breast cancer progression, recurrence, and metastasis. predominantly cytoplasmic HER2+ primary cells, but the expression subcellular localization of DUSPs, especially DUSP6, HER2-positive circulating tumor cells (CTCs) unknown. Here we used DEPArray system to identify isolate CTCs from metastatic triple negative (TNBC) patients performed single-cell NanoString analysis quantify pathway gene HER2-negative CTC populations. All TNBC...

10.3390/ijms20123080 article EN International Journal of Molecular Sciences 2019-06-24

Abstract Memory T cells exhibit transcriptional memory and “remember” their previous pathogenic encounter to increase transcription on re-infection. However, how this priming response is regulated unknown. Here we performed global FAIRE-seq profiling of chromatin accessibility in a human cell model. Primary activation induced persistent changes, secondary secondary-specific opening previously less accessible regions associated with enhanced expression memory-responsive genes. Increased...

10.1038/srep44825 article EN cc-by Scientific Reports 2017-03-20

Memory T cells are characterized by their rapid transcriptional programs upon re-stimulation. This memory response is facilitated permissive chromatin, but exactly how the epigenetic landscape in integrates incoming stimulatory signals remains poorly understood. By genome-wide ChIP-sequencing ex vivo human CD4(+) cells, here, we show that signaling enzyme, protein kinase C theta (PKC-θ) directly relays to chromatin binding transcriptional-memory-responsive genes induce activation. Flanked...

10.1242/jcs.181248 article EN cc-by Journal of Cell Science 2016-05-06
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