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Solvent A was 0.1% formic acid (FA) in ddH2O and solvent B was 80% ACN plus 0.1% FA. Peptides were injected in an aqueous 1% trifluoroacetic Acid (TFA) solution at a flow rate of 500 nL/min and were separated with 3%–60% gradients (110 min 3-21%, 18 min 21-30%, 5 min 30-60%), at a flow rate of 250 nL/min. The Q Exactive Plus instrument was operated in the data-dependent acquisition (DDA) mode. The acquired raw data were analyzed using the integrated MaxQuant software v.1.6.2.3 (Max Planck Institute of Biochemistry) and the Uniprot HUMAN (181029) databases."],"omics_type":["Proteomics"],"labhead":["Tiziana Bonaldi"],"instrument_platform":[""],"submission_type":["PARTIAL"],"labhead_affiliation":["European Institute of Oncology, Milan"],"species":["Homo Sapiens (human)"],"submitter_mail":["roberta.noberini@ieo.it"],"publication":["40408499 Marotta G, Osti D, Zaccheroni E, Costanza B, Faletti S, Marinaro A, Richichi C, Mesa D, Rodighiero S, Soriani C, Migliaccio E, Ruscitto F, Priami C, Sigismund S, Manetti F, Polli D, Beznusenko GV, Rusu MC, Favero F, Corà D, Silvestris DA, Gallo A, Gambino V, Alfieri F, Gandini S, Schmitt MJ, Gargiulo G, Noberini R, Bonaldi T, Pelicci G. Metabolic traits shape responses to LSD1-directed therapy in glioblastoma tumor-initiating cells. Sci Adv. 2025 11(21):eadt2724 10.1126/sciadv.adt2724"],"submitter_affiliation":["Istituto Europeo di Oncologia"],"submitter_country":["Italy"],"pubmed_abstract":["Lysine-specific histone demethylase 1A (LSD1) is an epigenetic regulator involved in various biological processes, including metabolic pathways. We demonstrated the therapeutic potential of its pharmacological inhibition in glioblastoma using DDP_38003 (LSD1i), which selectively targets tumor-initiating cells (TICs) by hampering their adaptability to stress. Through biological, metabolic, and omic approaches, we now show that LSD1i acts as an endoplasmic reticulum (ER) stressor, activating the integrated stress response and altering mitochondrial structure and function. These effects impair TICs' oxidative metabolism and generate reactive oxygen species, further amplifying cellular stress. LSD1i also impairs TICs' glycolytic activity, causing their metabolic decline. TICs with enhanced glycolysis benefit from LSD1-directed therapy. Conversely, metabolically silent TICs mantain ER and mitochondrial homeostasis, adapting to stress conditions, including LSD1i treatment. A dropout short hairpin RNA screening identifies postglycosylphosphatidylinositol attachment to proteins inositol deacylase 1 (PGAP1) as a mediator of resistance to LSD1i. Disruptions in ER and mitochondrial balance holds promise for improving LSD1-targeted therapy efficacy and overcoming treatment resistance."],"pubmed_title":["Metabolic traits shape responses to LSD1-directed therapy in glioblastoma tumor-initiating cells."],"pubmed_authors":["Marotta Giulia G, Osti Daniela D, Zaccheroni Elena E, Costanza Brunella B, Faletti Stefania S, Marinaro Adriana A, Richichi Cristina C, Mesa Deborah D, Rodighiero Simona S, Soriani Chiara C, Migliaccio Enrica E, Ruscitto Federica F, Priami Chiara C, Sigismund Sara S, Manetti Francesco F, Polli Dario D, Beznusenko Galina V GV, Rusu Mara-Camelia MC, Favero Francesco F, Corà Davide D, Silvestris Domenico A DA, Gallo Angela A, Gambino Valentina V, Alfieri Fabio F, Gandini Sara S, Schmitt Matthias J MJ, Gargiulo Gaetano G, Noberini Roberta R, Bonaldi Tiziana T, Pelicci Giuliana G"],"additional_accession":[]},"is_claimable":false,"name":"Intrinsic metabolic dependencies of glioblastoma tumor initiating cells dictate the sensitivity to LSD1-directed therapy","description":"Lysine-specific histone demethylase 1A (LSD1) is an epigenetic regulator involved in several biological processes, including metabolic pathways. We established the therapeutic benefit of its pharmacological inhibition in glioblastoma (GBM) using DDP_38003 (LSD1i), which selectively targets tumor-initiating cells (TICs) by hampering their adaptability to stress. Here, we demonstrate that LSD1i is a stress-inducing agent activating the integrated stress response by itself and triggering rearrangements of mitochondria which impact TICs oxidative 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