{"entity": "researcher", "timestamp": "2026-08-22T07:49:34.684Z", "family": "Papoutsoglou", "given": "Panagiotis", "initials": "P", "orcid": "0000-0003-2115-3500", "affiliations": ["Department of Medical Biochemistry and Microbiology, Science for Life Laboratory, Box 582, Biomedical Center, Uppsala University, Uppsala, Sweden.", "InInserm, Univ Rennes, UMR_S 1242, COSS (Chemistry, Oncogenesis Stress Signaling), Centre de Lutte contre le Cancer Eug\u00e8ne Marquis, Rennes, France."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/078d1572d1e449548f231a581860ed0a.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/078d1572d1e449548f231a581860ed0a"}}, "publications": [{"entity": "publication", "iuid": "304a9ea1a9ea4493ab1151c1a05f54f2", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/304a9ea1a9ea4493ab1151c1a05f54f2.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/304a9ea1a9ea4493ab1151c1a05f54f2"}}, "title": "The noncoding MIR100HG RNA enhances the autocrine function of transforming growth factor \u03b2 signaling.", "authors": [{"family": "Papoutsoglou", "given": "Panagiotis", "initials": "P", "orcid": "0000-0003-2115-3500", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/078d1572d1e449548f231a581860ed0a.json"}}, {"family": "Rodrigues-Junior", "given": "Dorival Mendes", "initials": "DM"}, {"family": "Mor\u00e9n", "given": "Anita", "initials": "A"}, {"family": "Bergman", "given": "Andrew", "initials": "A"}, {"family": "Pont\u00e9n", "given": "Fredrik", "initials": "F", "orcid": "0000-0003-0703-3940", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/9f5294424542413c9ba4432c839c2b63.json"}}, {"family": "Coulouarn", "given": "C\u00e9dric", "initials": "C", "orcid": "0000-0002-5692-9586", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/271ef91ebc7448fbaa500b32340528a0.json"}}, {"family": "Caja", "given": "Laia", "initials": "L", "orcid": "0000-0002-8786-8763", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/5f8e6b4e82274addbcaede8de73ad5d1.json"}}, {"family": "Heldin", "given": "Carl-Henrik", "initials": "CH", "orcid": "0000-0002-9508-896X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/5bca6678f5eb4baf853fca6ed5f9b726.json"}}, {"family": "Moustakas", "given": "Aristidis", "initials": "A", "orcid": "0000-0001-9131-3827", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/f11771bffabf4da6a2a5e2668c7c7c2d.json"}}], "type": "journal article", "published": "2021-05-00", "journal": {"title": "Oncogene", "issn": "1476-5594", "volume": "40", "issue": "21", "pages": "3748-3765", "issn-l": "0950-9232"}, "abstract": "Activation of the transforming growth factor \u03b2 (TGF\u03b2) pathway modulates the expression of genes involved in cell growth arrest, motility, and embryogenesis. An expression screen for long noncoding RNAs indicated that TGF\u03b2 induced mir-100-let-7a-2-mir-125b-1 cluster host gene (MIR100HG) expression in diverse cancer types, thus confirming an earlier demonstration of TGF\u03b2-mediated transcriptional induction of MIR100HG in pancreatic adenocarcinoma. MIR100HG depletion attenuated TGF\u03b2 signaling, expression of TGF\u03b2-target genes, and TGF\u03b2-mediated cell cycle arrest. Moreover, MIR100HG silencing inhibited both normal and cancer cell motility and enhanced the cytotoxicity of cytostatic drugs. MIR100HG overexpression had an inverse impact on TGF\u03b2 signaling responses. Screening for downstream effectors of MIR100HG identified the ligand TGF\u03b21. MIR100HG and TGFB1 mRNA formed ribonucleoprotein complexes with the RNA-binding protein HuR, promoting TGF\u03b21 cytokine secretion. In addition, TGF\u03b2 regulated let-7a-2-3p, miR-125b-5p, and miR-125b-1-3p expression, all encoded by MIR100HG intron-3. Certain intron-3 miRNAs may be involved in TGF\u03b2/SMAD-mediated responses (let-7a-2-3p) and others (miR-100, miR-125b) in resistance to cytotoxic drugs mediated by MIR100HG. In support of a model whereby TGF\u03b2 induces MIR100HG, which then enhances TGF\u03b21 secretion, analysis of human carcinomas showed that MIR100HG expression correlated with expression of TGFB1 and its downstream extracellular target TGFBI. Thus, MIR100HG controls the magnitude of TGF\u03b2 signaling via TGF\u03b21 autoinduction and secretion in carcinomas.", "doi": "10.1038/s41388-021-01803-8", "pmid": "33941855", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC8154591"}, {"db": "pii", "key": "10.1038/s41388-021-01803-8"}], "notes": [], "created": "2026-08-20T08:48:29.471Z", "modified": "2026-08-20T08:48:29.596Z"}, {"entity": "publication", "iuid": "081ec524c925462798f54d544899e3ee", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/081ec524c925462798f54d544899e3ee.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/081ec524c925462798f54d544899e3ee"}}, "title": "Long non-coding RNAs and TGF-\u03b2 signaling in cancer.", "authors": [{"family": "Papoutsoglou", "given": "Panagiotis", "initials": "P", "orcid": "0000-0003-2115-3500", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/078d1572d1e449548f231a581860ed0a.json"}}, {"family": "Moustakas", "given": "Aristidis", "initials": "A", "orcid": "0000-0001-9131-3827", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/f11771bffabf4da6a2a5e2668c7c7c2d.json"}}], "type": "journal article", "published": "2020-08-00", "journal": {"title": "Cancer Sci.", "issn": "1349-7006", "volume": "111", "issue": "8", "pages": "2672-2681", "issn-l": "1347-9032"}, "abstract": "Cancer is driven by genetic mutations in oncogenes and tumor suppressor genes and by cellular events that develop a misregulated molecular microenvironment in the growing tumor tissue. The tumor microenvironment is guided by the excessive action of specific cytokines including transforming growth factor-\u03b2 (TGF-\u03b2), which normally controls embryonic development and the homeostasis of young or adult tissues. As a consequence of the genetic alterations generating a given tumor, TGF-\u03b2 can preserve its homeostatic function and attempt to limit neoplastic expansion, whereas, once the tumor has progressed to an aggressive stage, TGF-\u03b2 can synergize with various oncogenic stimuli to facilitate tumor invasiveness and metastasis. TGF-\u03b2 signaling mechanisms via Smad proteins, various ubiquitin ligases, and protein kinases are relatively well understood. Such mechanisms regulate the expression of genes encoding proteins or non-coding RNAs. Among non-coding RNAs, much has been understood regarding the regulation and function of microRNAs, whereas the role of long non-coding RNAs is still emerging. This article emphasizes TGF-\u03b2 signaling mechanisms leading to the regulation of non-coding genes, the function of such non-coding RNAs as regulators of TGF-\u03b2 signaling, and the contribution of these mechanisms in specific hallmarks of cancer.", "doi": "10.1111/cas.14509", "pmid": "32485023", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC7419046"}], "notes": [], "created": "2026-08-20T11:17:29.750Z", "modified": "2026-08-20T11:17:29.807Z"}]}