{"entity": "researcher", "timestamp": "2026-09-26T03:41:08.419Z", "family": "Maturi", "given": "Varun", "initials": "V", "orcid": "0000-0003-1177-0839", "affiliations": ["Department of Medical Biochemistry and Microbiology, Science for Life Laboratory, Uppsala University, PO Box 582, SE-751 23, Uppsala, Sweden.", "Ludwig Institute for Cancer Research, Science for Life Laboratory, Uppsala University, PO Box 595, SE-751 24, Uppsala, Sweden."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/fdfcc911f5f148008bff3cadbc093df7.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/fdfcc911f5f148008bff3cadbc093df7"}}, "publications": [{"entity": "publication", "iuid": "8e513fd633a245638135c84bbf5644dd", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/8e513fd633a245638135c84bbf5644dd.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/8e513fd633a245638135c84bbf5644dd"}}, "title": "Loss of SNAI1 induces cellular plasticity in invasive triple-negative breast cancer cells.", "authors": [{"family": "Tsirigoti", "given": "Chrysoula", "initials": "C"}, {"family": "Ali", "given": "Mohamad Moustafa", "initials": "MM", "orcid": "0000-0002-4902-0550", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/805bc529dce14a4f8ea863e2a26a312a.json"}}, {"family": "Maturi", "given": "Varun", "initials": "V", "orcid": "0000-0003-1177-0839", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/fdfcc911f5f148008bff3cadbc093df7.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": "2022-09-28", "journal": {"title": "Cell Death Dis", "issn": "2041-4889", "volume": "13", "issue": "9", "pages": "832", "issn-l": "2041-4889"}, "abstract": "The transcription factor SNAI1 mediates epithelial-mesenchymal transition, fibroblast activation and controls inter-tissue migration. High SNAI1 expression characterizes metastatic triple-negative breast carcinomas, and its knockout by CRISPR/Cas9 uncovered an epithelio-mesenchymal phenotype accompanied by reduced signaling by the cytokine TGF\u03b2. The SNAI1 knockout cells exhibited plasticity in differentiation, drifting towards the luminal phenotype, gained stemness potential and could differentiate into acinar mammospheres in 3D culture. Loss of SNAI1 de-repressed the transcription factor FOXA1, a pioneering factor of mammary luminal progenitors. FOXA1 induced a specific gene program, including the androgen receptor (AR). Inhibiting AR via a specific antagonist regenerated the basal phenotype and blocked acinar differentiation. Thus, loss of SNAI1 in the context of triple-negative breast carcinoma cells promotes an intermediary luminal progenitor phenotype that gains differentiation plasticity based on the dual transcriptional action of FOXA1 and AR. This function of SNAI1 provides means to separate cell invasiveness from progenitor cell de-differentiation as independent cellular programs.", "doi": "10.1038/s41419-022-05280-z", "pmid": "36171192", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC9519755"}, {"db": "pii", "key": "10.1038/s41419-022-05280-z"}], "notes": [], "created": "2026-09-23T10:10:04.223Z", "modified": "2026-09-23T10:48:23.112Z"}, {"entity": "publication", "iuid": "86062ba0bb3d47e38630a529554e2b0c", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/86062ba0bb3d47e38630a529554e2b0c.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/86062ba0bb3d47e38630a529554e2b0c"}}, "title": "Systemic and specific effects of antihypertensive and lipid-lowering medication on plasma protein biomarkers for cardiovascular diseases.", "authors": [{"family": "Enroth", "given": "Stefan", "initials": "S", "orcid": "0000-0002-5056-9137", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/ae9be8ef3b1145239a4e0231e2a148cd.json"}}, {"family": "Maturi", "given": "Varun", "initials": "V", "orcid": "0000-0003-1177-0839", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/fdfcc911f5f148008bff3cadbc093df7.json"}}, {"family": "Berggrund", "given": "Malin", "initials": "M"}, {"family": "Enroth", "given": "Sofia Bosdotter", "initials": "SB"}, {"family": "Moustakas", "given": "Aristidis", "initials": "A"}, {"family": "Johansson", "given": "\u00c5sa", "initials": "\u00c5", "orcid": "0000-0002-2915-4498", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a0bac3e1e64949fcbac4b4d839e1144d.json"}}, {"family": "Gyllensten", "given": "Ulf", "initials": "U"}], "type": "journal article", "published": "2018-04-03", "journal": {"title": "Sci Rep", "issn": "2045-2322", "volume": "8", "issue": "1", "pages": "5531", "issn-l": "2045-2322"}, "abstract": "A large fraction of the adult population is on lifelong medication for cardiovascular disorders, but the metabolic consequences are largely unknown. This study determines the effects of common anti-hypertensive and lipid lowering drugs on circulating plasma protein biomarkers. We studied 425 proteins in plasma together with anthropometric and lifestyle variables, and the genetic profile in a cross-sectional cohort. We found 8406 covariate-protein associations, and a two-stage GWAS identified 17253 SNPs to be associated with 109 proteins. By computationally removing variation due to lifestyle and genetic factors, we could determine that medication, per se, affected the abundance levels of 35.7% of the plasma proteins. Medication either affected a single, a few, or a large number of protein, and were found to have a negative or positive influence on known disease pathways and biomarkers. Anti-hypertensive or lipid lowering drugs affected 33.1% of the proteins. Angiotensin-converting enzyme inhibitors showed the strongest lowering effect by decreasing plasma levels of myostatin. Cell-culture experiments showed that angiotensin-converting enzyme inhibitors reducted myostatin RNA levels. Thus, understanding the effects of lifelong medication on the plasma proteome is important both for sharpening the diagnostic precision of protein biomarkers and in disease management.", "doi": "10.1038/s41598-018-23860-y", "pmid": "29615742", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC5882890"}, {"db": "pii", "key": "10.1038/s41598-018-23860-y"}], "notes": [], "created": "2018-12-05T12:44:18.207Z", "modified": "2026-09-23T09:29:17.355Z"}]}