Proteomic Investigation of the Role of Nucleostemin in Nucleophosmin-Mutated OCI-AML 3 Cell Line.

{"sci_version": "1.2", "schema": "https://corpus.bntrg.co.uk/sci/1.0/sci.schema.json", "id": "pmid:35886999", "kind": "science-record", "revision": 3, "content_hash": "sha256:9b49a0b8184b0f95e5d479bb7938136bde66743f71cb2be4c9fb9b6d8d86cb55", "created_at": "2026-11-01T18:14:58Z", "updated_at": "2026-11-01T21:28:29Z", "generator": {"name": "corpus-assay-engine", "run_id": "reading-sci-2026-11-01"}, "paper": {"state": "complete", "title": "Proteomic Investigation of the Role of Nucleostemin in Nucleophosmin-Mutated OCI-AML 3 Cell Line.", "doi": "10.3390/ijms23147655", "pmid": "35886999", "authors": ["Ilaria Cela", "Maria Concetta Cufaro", "Maurine Fucito", "Damiana Pieragostino", "Paola Lanuti", "Michele Sallese", "Piero Del Boccio", "Adele Di Matteo", "Nerino Allocati", "Vincenzo De Laurenzi", "Luca Federici"], "journal": "International journal of molecular sciences", "year": 2022, "abstract": "Nucleostemin (NS; a product of the GNL3 gene) is a nucleolar-nucleoplasm shuttling GTPase whose levels are high in stem cells and rapidly decrease upon differentiation. NS levels are also high in several solid and hematological neoplasms, including acute myeloid leukaemia (AML). While a role in telomere maintenance, response to stress stimuli and favoring DNA repair has been proposed in solid cancers, little or no information is available as to the role of nucleostemin in AML. Here, we investigate this issue via a proteomics approach. We use as a model system the OCI-AML 3 cell line harboring a heterozygous mutation at the NPM1 gene, which is the most frequent driver mutation in AML (approximately 30% of total AML cases). We show that NS is highly expressed in this cell line, and, contrary to what has previously been shown in other cancers, that its presence is dispensable for cell growth and viability. However, proteomics analysis of the OCI-AML 3 cell line before and after nucleostemin (NS) silencing showed several effects on different biological functions, as highlighted by ingenuity pathway analysis (IPA). In particular, we report an effect of down-regulating DNA repair through homologous recombination, and we confirmed a higher DNA damage rate in OCI-AML 3 cells when NS is depleted, which considerably increases upon stress induced by the topoisomerase II inhibitor etoposide. The data used are available via ProteomeXchange with the identifier PXD034012.", "claims": [{"id": "claim-method", "statement": "Among all the common proteins analyzed, 133 significant differentially expressed proteins (p-value < 0.05) were determined via t-test.", "kind": "methodological", "target": null, "evidence": [{"asset": "source:pmid:35886999", "locator": "sections[4] \"2.2. Comparative Proteomics Analysis of OCI-AML 3 Cell Lines\" paragraph 2", "quote": "Among all the common proteins analyzed, 133 significant differentially expressed proteins (p-value < 0.05) were determined via t-test."}], "state": "complete"}, {"id": "claim-data-access", "statement": "The data used are available via ProteomeXchange with the identifier PXD034012.", "kind": "methodological", "target": null, "evidence": [{"asset": "source:pmid:35886999", "locator": "sections[0] \"Abstract\" paragraph 1", "quote": "The data used are available via ProteomeXchange with the identifier PXD034012."}], "state": "complete"}, {"id": "claim-target-result", "statement": "NS silencing down-regulates DNA repair through homologous recombination and increases DNA damage in OCI-AML 3 cells, with the effect further increased under etoposide stress.", "kind": "qualitative", "target": null, "evidence": [{"asset": "source:pmid:35886999", "locator": "sections[0] \"Abstract\" paragraph 1", "quote": "In particular, we report an effect of down-regulating DNA repair through homologous recombination, and we confirmed a higher DNA damage rate in OCI-AML 3 cells when NS is depleted, which considerably increases upon stress induced by the topoisomerase II inhibitor etoposide."}], "state": "complete"}], "gaps": []}, "experiment": {"state": "complete", "objective": "NS silencing down-regulates DNA repair through homologous recombination and increases DNA damage in OCI-AML 3 cells, with the effect further increased under etoposide stress.", "steps": [{"id": "read_published_estimate", "order": 1, "name": "Read the published estimate from the source", "kind": "other", "state": "complete", "blocked_on": null, "description": "The claim, method and evidence span published with the source article.", "duration_hours": null, "parameters": {}, "inputs": ["source:pmid:35886999"], "outputs": ["the published estimate and its evidence"], "instruments": [], "reagents": []}, {"id": "obtain_source_data", "order": 2, "name": "Obtain the source data from the named repository", "kind": "data-preparation", "state": "complete", "blocked_on": null, "description": "The GEO series accession resolves and its sample accessions are listed. 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