{"entity": "researcher", "timestamp": "2026-08-23T22:24:34.638Z", "family": "Olasz", "given": "Judit", "initials": "J", "orcid": "0000-0002-6740-7484", "affiliations": ["Department of Pathogenetics, National Institute of Oncology, 1122 Budapest, Hungary."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/b7981a52c764499480110c95da890a6c.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/b7981a52c764499480110c95da890a6c"}}, "publications": [{"entity": "publication", "iuid": "d8e1b30f4183465f94365c387ca2e861", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/d8e1b30f4183465f94365c387ca2e861.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/d8e1b30f4183465f94365c387ca2e861"}}, "title": "Reprogrammed transsulfuration promotes basal-like breast tumor progression via realigning cellular cysteine persulfidation.", "authors": [{"family": "Erd\u00e9lyi", "given": "Katalin", "initials": "K", "orcid": "0000-0001-8802-1292", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/de4eade234384ce8a2d1e64e0d98a6a6.json"}}, {"family": "Ditr\u00f3i", "given": "Tam\u00e1s", "initials": "T"}, {"family": "Johansson", "given": "Henrik J", "initials": "HJ"}, {"family": "Czikora", "given": "\u00c1gnes", "initials": "\u00c1"}, {"family": "Balog", "given": "No\u00e9mi", "initials": "N", "orcid": "0000-0001-6481-6576", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/fafc71642a174af8830c9fc15e980fe6.json"}}, {"family": "Silwal-Pandit", "given": "Laxmi", "initials": "L"}, {"family": "Ida", "given": "Tomoaki", "initials": "T"}, {"family": "Olasz", "given": "Judit", "initials": "J", "orcid": "0000-0002-6740-7484", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/b7981a52c764499480110c95da890a6c.json"}}, {"family": "Hajd\u00fa", "given": "Dorottya", "initials": "D"}, {"family": "M\u00e1trai", "given": "Zolt\u00e1n", "initials": "Z", "orcid": "0000-0001-8160-7100", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/8140edc270154a7c81db771ea2ae9e0e.json"}}, {"family": "Csuka", "given": "Orsolya", "initials": "O"}, {"family": "Uchida", "given": "Koji", "initials": "K"}, {"family": "T\u00f3v\u00e1ri", "given": "J\u00f3zsef", "initials": "J"}, {"family": "Engebraten", "given": "Olav", "initials": "O"}, {"family": "Akaike", "given": "Takaaki", "initials": "T", "orcid": "0000-0002-0623-1710", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/5180e9b3deea4d77875e1d708939e1b9.json"}}, {"family": "B\u00f8rresen Dale", "given": "Anne-Lise", "initials": "AL"}, {"family": "K\u00e1sler", "given": "Mikl\u00f3s", "initials": "M"}, {"family": "Lehti\u00f6", "given": "Janne", "initials": "J"}, {"family": "Nagy", "given": "P\u00e9ter", "initials": "P", "orcid": "0000-0003-3393-235X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/3006b619352e467f904743ceece413a2.json"}}], "type": "journal article", "published": "2021-11-09", "journal": {"title": "Proc. Natl. Acad. Sci. U.S.A.", "issn": "1091-6490", "volume": "118", "issue": "45", "issn-l": "0027-8424"}, "abstract": "Basal-like breast cancer (BLBC) is the most aggressive subtype of breast tumors with poor prognosis and limited molecular-targeted therapy options. We show that BLBC cells have a high Cys demand and reprogrammed Cys metabolism. Patient-derived BLBC tumors from four different cohorts exhibited elevated expression of the transsulfuration enzyme cystathione \u03b2-synthetase (CBS). CBS silencing (shCBS) made BLBC cells less invasive, proliferate slower, more vulnerable to oxidative stress and cystine (CySSCy) deprivation, prone to ferroptosis, and less responsive to HIF1-\u03b1 activation under hypoxia. shCBS xenograft tumors grew slower than controls and exhibited impaired angiogenesis and larger necrotic areas. Sulfur metabolite profiling suggested that realigned sulfide/persulfide-inducing functions of CBS are important in BLBC tumor progression. Supporting this, the exclusion of serine, a substrate of CBS for producing Cys but not for producing sulfide/persulfide, did not exacerbate CySSCy deprivation-induced ferroptosis in shCBS BLBC cells. Impaired Tyr phosphorylation was detected in shCBS cells and xenografts, likely due to persulfidation-inhibited phosphatase functions. Overexpression of cystathione \u03b3-lyase (CSE), which can also contribute to cellular sulfide/persulfide production, compensated for the loss of CBS activities, and treatment of shCBS xenografts with a CSE inhibitor further blocked tumor growth. Glutathione and protein-Cys levels were not diminished in shCBS cells or xenografts, but levels of Cys persulfidation and the persulfide-catabolizing enzyme ETHE1 were suppressed. Finally, expression of enzymes of the oxidizing Cys catabolism pathway was diminished, but expression of the persulfide-producing CARS2 was elevated in human BLBC tumors. Hence, the persulfide-producing pathways are major targetable determinants of BLBC pathology that could be therapeutically exploited.", "doi": "10.1073/pnas.2100050118", "pmid": "34737229", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC8609449"}, {"db": "pii", "key": "2100050118"}], "notes": [], "created": "2026-08-20T09:30:54.955Z", "modified": "2026-08-20T09:30:55.201Z"}]}