{"entity": "researcher", "timestamp": "2026-08-22T07:47:41.179Z", "family": "Morikawa", "given": "Masato", "initials": "M", "orcid": "0000-0002-6191-7176", "affiliations": ["Department of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, Japan."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/b9bdbfae5ccc46abadd9bda329dfce14.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/b9bdbfae5ccc46abadd9bda329dfce14"}}, "publications": [{"entity": "publication", "iuid": "4b31be3bc722411592daf9d2f392004a", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/4b31be3bc722411592daf9d2f392004a.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/4b31be3bc722411592daf9d2f392004a"}}, "title": "PRRX1 induced by BMP signaling decreases tumorigenesis by epigenetically regulating glioma-initiating cell properties via DNA methyltransferase 3A.", "authors": [{"family": "Tanabe", "given": "Ryo", "initials": "R"}, {"family": "Miyazono", "given": "Kohei", "initials": "K", "orcid": "0000-0001-7341-0172", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/88b0a85433264e96a3c4f2e27ca0e3f7.json"}}, {"family": "Todo", "given": "Tomoki", "initials": "T"}, {"family": "Saito", "given": "Nobuhito", "initials": "N"}, {"family": "Iwata", "given": "Caname", "initials": "C", "orcid": "0000-0003-1957-711X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/724ab44ad3ef45018d6a2390b912af6e.json"}}, {"family": "Komuro", "given": "Akiyoshi", "initials": "A"}, {"family": "Sakai", "given": "Satoshi", "initials": "S"}, {"family": "Raja", "given": "Erna", "initials": "E"}, {"family": "Koinuma", "given": "Daizo", "initials": "D", "orcid": "0000-0001-5611-2122", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/14df9a6f4d4c4346836c083482a0b563.json"}}, {"family": "Morikawa", "given": "Masato", "initials": "M", "orcid": "0000-0002-6191-7176", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/b9bdbfae5ccc46abadd9bda329dfce14.json"}}, {"family": "Westermark", "given": "Bengt", "initials": "B"}, {"family": "Heldin", "given": "Carl-Henrik", "initials": "CH"}], "type": "journal article", "published": "2022-01-00", "journal": {"title": "Mol Oncol", "issn": "1878-0261", "volume": "16", "issue": "1", "pages": "269-288", "issn-l": "1574-7891"}, "abstract": "Glioma-initiating cells (GICs), a major source of glioblastoma recurrence, are characterized by the expression of neural stem cell markers and the ability to grow by forming nonadherent spheres under serum-free conditions. Bone morphogenetic proteins (BMPs), members of the transforming growth factor-\u03b2 family, induce differentiation of GICs and suppress their tumorigenicity. However, the mechanisms underlying the BMP-induced loss of GIC stemness have not been fully elucidated. Here, we show that paired related homeobox 1 (PRRX1) induced by BMPs decreases the CD133-positive GIC population and inhibits tumorigenic activity of GICs in vivo. Of the two splice isoforms of PRRX1, the longer isoform, pmx-1b, but not the shorter isoform, pmx-1a, induces GIC differentiation. Upon BMP stimulation, pmx-1b interacts with the DNA methyltransferase DNMT3A and induces promoter methylation of the PROM1 gene encoding CD133. Silencing DNMT3A maintains PROM1 expression and increases the CD133-positive GIC population. Thus, pmx-1b promotes loss of stem cell-like properties of GICs through region-specific epigenetic regulation of CD133 expression by recruiting DNMT3A, which is associated with decreased tumorigenicity of GICs.", "doi": "10.1002/1878-0261.13051", "pmid": "34214250", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC8732353"}], "notes": [], "created": "2026-08-20T06:25:38.587Z", "modified": "2026-08-20T06:25:38.835Z"}, {"entity": "publication", "iuid": "af4c437c1db64006ae2b1d43d1be789a", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/af4c437c1db64006ae2b1d43d1be789a.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/af4c437c1db64006ae2b1d43d1be789a"}}, "title": "TGF\u03b2 and EGF signaling orchestrates the AP-1- and p63 transcriptional regulation of breast cancer invasiveness.", "authors": [{"family": "Sundqvist", "given": "Anders", "initials": "A", "orcid": "0000-0001-9542-0881", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/0bd49e77450e4d5bb924813d1565a8dd.json"}}, {"family": "Vasilaki", "given": "Eleftheria", "initials": "E"}, {"family": "Voytyuk", "given": "Oleksandr", "initials": "O"}, {"family": "Bai", "given": "Yu", "initials": "Y"}, {"family": "Morikawa", "given": "Masato", "initials": "M", "orcid": "0000-0002-6191-7176", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/b9bdbfae5ccc46abadd9bda329dfce14.json"}}, {"family": "Moustakas", "given": "Aristidis", "initials": "A"}, {"family": "Miyazono", "given": "Kohei", "initials": "K"}, {"family": "Heldin", "given": "Carl-Henrik", "initials": "CH", "orcid": "0000-0002-9508-896X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/5bca6678f5eb4baf853fca6ed5f9b726.json"}}, {"family": "Ten Dijke", "given": "Peter", "initials": "P"}, {"family": "van Dam", "given": "Hans", "initials": "H"}], "type": "journal article", "published": "2020-05-00", "journal": {"title": "Oncogene", "issn": "1476-5594", "volume": "39", "issue": "22", "pages": "4436-4449", "issn-l": "0950-9232"}, "abstract": "Activator protein (AP)-1 transcription factors are essential elements of the pro-oncogenic functions of transforming growth factor-\u03b2 (TGF\u03b2)-SMAD signaling. Here we show that in multiple HER2+ and/or EGFR+ breast cancer cell lines these AP-1-dependent tumorigenic properties of TGF\u03b2 critically rely on epidermal growth factor receptor (EGFR) activation and expression of the \u0394N isoform of transcriptional regulator p63. EGFR and \u0394Np63 enabled and/or potentiated the activation of a subset of TGF\u03b2-inducible invasion/migration-associated genes, e.g., ITGA2, LAMB3, and WNT7A/B, and enhanced the recruitment of SMAD2/3 to these genes. The TGF\u03b2- and EGF-induced binding of SMAD2/3 and JUNB to these gene loci was accompanied by p63-SMAD2/3 and p63-JUNB complex formation. p63 and EGFR were also found to strongly potentiate TGF\u03b2 induction of AP-1 proteins and, in particular, FOS family members. Ectopic overexpression of FOS could counteract the decrease in TGF\u03b2-induced gene activation after p63 depletion. p63 is also involved in the transcriptional regulation of heparin binding (HB)-EGF and EGFR genes, thereby establishing a self-amplification loop that facilitates and empowers the pro-invasive functions of TGF\u03b2. These cooperative pro-oncogenic functions of EGFR, AP-1, p63, and TGF\u03b2 were efficiently inhibited by clinically relevant chemical inhibitors. Our findings may, therefore, be of importance for therapy of patients with breast cancers with an activated EGFR-RAS-RAF pathway.", "doi": "10.1038/s41388-020-1299-z", "pmid": "32350443", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC7253358"}, {"db": "pii", "key": "10.1038/s41388-020-1299-z"}], "notes": [], "created": "2026-08-20T08:48:27.198Z", "modified": "2026-08-20T08:48:27.297Z"}]}