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      The Diverse Consequences of FOXC1 Deregulation in Cancer

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          Abstract

          Forkhead box C1 (FOXC1) is a transcription factor with essential roles in mesenchymal lineage specification and organ development during normal embryogenesis. In keeping with these developmental properties, mutations that impair the activity of FOXC1 result in the heritable Axenfeld-Rieger Syndrome and other congenital disorders. Crucially, gain of FOXC1 function is emerging as a recurrent feature of malignancy; FOXC1 overexpression is now documented in more than 16 cancer types, often in association with an unfavorable prognosis. This review explores current evidence for FOXC1 deregulation in cancer and the putative mechanisms by which FOXC1 confers its oncogenic effects.

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          The androgen receptor cistrome is extensively reprogrammed in human prostate tumorigenesis

          Mark M. Pomerantz, Fugen Li, David Takeda … (2015)
          Master transcription factors interact with DNA to establish cell-type identity and to regulate gene expression in mammalian cells 1,2 . The genome-wide map of these transcription factor binding sites has been termed the cistrome 3 . Here we show that the androgen receptor (AR) cistrome undergoes extensive reprogramming during prostate epithelial transformation in man. Using human prostate tissue, we observed a core set of AR binding sites that are consistently reprogrammed in tumors. FOXA1 and HOXB13, co-localized with the reprogrammed AR sites in human tumor tissue. Introduction of FOXA1 and HOXB13 into an immortalized prostate cell line reprogrammed the AR cistrome to resemble that of a prostate tumor, functionally linking these specific factors to AR reprogramming. These findings offer mechanistic insights into a key set of events that drive normal prostate epithelium towards transformation and establish the centrality of epigenetic reprogramming in human prostate tumorigenesis.
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            The Pioneer Transcription Factor FoxA Maintains an Accessible Nucleosome Configuration at Enhancers for Tissue-Specific Gene Activation.

            Makiko Iwafuchi-Doi, Greg Donahue, Akshay Kakumanu … (2016)
            Nuclear DNA wraps around core histones to form nucleosomes, which restricts the binding of transcription factors to gene regulatory sequences. Pioneer transcription factors can bind DNA sites on nucleosomes and initiate gene regulatory events, often leading to the local opening of chromatin. However, the nucleosomal configuration of open chromatin and the basis for its regulation is unclear. We combined low and high levels of micrococcal nuclease (MNase) digestion along with core histone mapping to assess the nucleosomal configuration at enhancers and promoters in mouse liver. We find that MNase-accessible nucleosomes, bound by transcription factors, are retained more at liver-specific enhancers than at promoters and ubiquitous enhancers. The pioneer factor FoxA displaces linker histone H1, thereby keeping enhancer nucleosomes accessible in chromatin and allowing other liver-specific transcription factors to bind and stimulate transcription. Thus, nucleosomes are not exclusively repressive to gene regulation when they are retained with, and exposed by, pioneer factors.
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              Steroid Receptors Reprogram FoxA1 Occupancy through Dynamic Chromatin Transitions.

              Erin Swinstead, Tina Miranda, Ville Paakinaho … (2016)
              The estrogen receptor (ER), glucocorticoid receptor (GR), and forkhead box protein 1 (FoxA1) are significant factors in breast cancer progression. FoxA1 has been implicated in establishing ER-binding patterns though its unique ability to serve as a pioneer factor. However, the molecular interplay between ER, GR, and FoxA1 requires further investigation. Here we show that ER and GR both have the ability to alter the genomic distribution of the FoxA1 pioneer factor. Single-molecule tracking experiments in live cells reveal a highly dynamic interaction of FoxA1 with chromatin in vivo. Furthermore, the FoxA1 factor is not associated with detectable footprints at its binding sites throughout the genome. These findings support a model wherein interactions between transcription factors and pioneer factors are highly dynamic. Moreover, at a subset of genomic sites, the role of pioneer can be reversed, with the steroid receptors serving to enhance binding of FoxA1.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cancers (Basel)
                Journal ID (iso-abbrev): Cancers (Basel)
                Journal ID (publisher-id): cancers
                Title: Cancers
                Publisher: MDPI
                ISSN (Electronic): 2072-6694
                Publication date (Electronic): 05 February 2019
                Publication date Collection: February 2019
                Volume: 11
                Issue: 2
                Electronic Location Identifier: 184
                Affiliations
                Leukaemia Biology Laboratory, Cancer Research UK Manchester Institute, The University of Manchester, Manchester M20 4JG, UK; niall.gilding@ 123456cruk.manchester.ac.uk
                Author notes
                [* ]Correspondence: tim.somervaille@ 123456cruk.manchester.ac.uk ; Tel.: +44-161-306-3240
                Author information
                https://orcid.org/0000-0002-3540-0712
                https://orcid.org/0000-0002-9188-4379
                Article
                Publisher ID: cancers-11-00184
                DOI: 10.3390/cancers11020184
                PMC ID: 6406774
                PubMed ID: 30764547
                SO-VID: 5a756fd4-cba0-43b0-94c2-88e19e211a21
                Copyright © © 2019 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 05 January 2019
                Date accepted : 30 January 2019
                Categories
                Subject: Review

                Keywords: epigenetics,transcription factor,epithelial-mesenchymal transition,metastasis,cellular reprogramming,pioneer factor
                Data availability:
                Keywords: epigenetics, transcription factor, epithelial-mesenchymal transition, metastasis, cellular reprogramming, pioneer factor

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