{"id":"d68eb603-85b7-51a3-8d97-a99b981503f0","stable_key":"research:kmsb-hdac","predicate":"inhibits","statement":"Keto-methylselenobutyrate inhibits HDAC activity in the reported enzyme/cancer-cell experiments.","claim_class":"mechanistic","status":"source_derived_draft","evidence_grade":"literature_reviewed:direct_experimental","direction":"negative","is_public":true,"mechanism_event_id":"e49e88e2-5964-5dd1-9eca-c78bf22ed09a","mechanism_event_label":"This second distinct metabolite can also inhibit tested histone-deacetylase activity.","subject":{"id":"fca7a11e-fd30-5d27-aa22-6e2c218a8284","slug":"keto-methylselenobutyrate","display_name":"KMSB","entity_type_key":"small_molecule"},"object":{"id":"256770e5-bbe5-55be-8b4b-e697a269d391","slug":"hdac-activity","display_name":"histone deacetylase activity","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"e49e88e2-5964-5dd1-9eca-c78bf22ed09a","stable_key":"research:kmsb-hdac","event_type":"enzyme_inhibition","label":"This second distinct metabolite can also inhibit tested histone-deacetylase activity.","description":"Keto-methylselenobutyrate inhibits HDAC activity in the reported enzyme/cancer-cell experiments.","status":"active","compartment":null,"participants":[{"entity":{"id":"fca7a11e-fd30-5d27-aa22-6e2c218a8284","slug":"keto-methylselenobutyrate","display_name":"KMSB","entity_type_key":"small_molecule"},"role":"subject","stoichiometry":null,"state_label":"","sequence_order":0,"notes":""},{"entity":{"id":"256770e5-bbe5-55be-8b4b-e697a269d391","slug":"hdac-activity","display_name":"histone deacetylase activity","entity_type_key":"cellular_process"},"role":"object","stoichiometry":null,"state_label":"","sequence_order":1,"notes":""}]},"contexts":[{"dimension":"cell_type","value_text":"Cancer cells and biochemical systems","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_model","value_text":"Enzyme and human cancer-cell assays","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"Not interchangeable with parent compounds or proof of dietary cancer prevention.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"organism","value_text":"Homo sapiens","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"1e0fb4a1-841e-58d7-91d0-264718620c2a","evidence_kind":"curated_literature_summary","locator":"lines 1444-1454","start_line":1444,"end_line":1454,"excerpt":"## kmsb-hdac\n\nThis second distinct metabolite can also inhibit tested histone-deacetylase activity.\n\nKeto-methylselenobutyrate inhibits HDAC activity in the reported enzyme/cancer-cell experiments.\n\nOrganism: Homo sapiens\nCell type: Cancer cells and biochemical systems\nExperimental model: Enzyme and human cancer-cell assays\nLimitations: Not interchangeable with parent compounds or proof of dietary cancer prevention.\nPrimary reference: [α-Keto acid metabolites of organoselenium compounds inhibit histone deacetylase activity in human colon cancer cells](https://pmc.ncbi.nlm.nih.gov/articles/PMC2718078/)","model_system":"Enzyme and human cancer-cell assays","directness":"author_interpretation","verification_status":"secondary_verified","notes":"Curated summary; inspect the linked primary papers for original methods and results.","relationship":"supports","weight":1.0,"link_notes":"","source":{"id":"4f892f13-06ea-5199-a33c-a703f35c80ae","stable_key":"selenium-research-2026-09-17","title":"Selenium: literature corrections and mechanism additions","document_type":"curated_literature_review","citation_label":"Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually","file_path":"","sha256":"0b818b10c1c7120e5caf7f4d4019d7bd025d745692e424f515d3ef903c9ab7f3","revision_id":"80984e03-5f0f-5877-8094-afef7637444e","review_status":"secondary_verified","notes":"Secondary curated summaries of primary experiments, with explicit models and limitations. Not archived primary full text."}}],"relations":[],"conflicts":[],"corrections":[{"id":"ee8136ef-7cee-57fa-b694-f001e0df604e","title":"HDAC effects need chemically distinct selenium metabolites","kind":"qualification","status":"qualified","why":"MSP/KMSB inhibition evidence cannot be transferred to methylselenol or parent compounds as though they were the same species.","resolution":"Keep compound-specific claims; direct methylselenol HDAC inhibition is unestablished by these studies, not disproved in every context.","created_at":"2026-09-17 07:19:34","record_type":"qualification","display_label":"Source qualification","record_url":"/corrections/ee8136ef-7cee-57fa-b694-f001e0df604e","literature_review":{"revision_id":"80984e03-5f0f-5877-8094-afef7637444e","start_line":1683,"end_line":1688,"papers":[{"paper_key":"nian-2009","title":"α-Keto acid metabolites of organoselenium compounds inhibit histone deacetylase activity in human colon cancer cells","url":"https://pmc.ncbi.nlm.nih.gov/articles/PMC2718078/","doi":"10.1093/carcin/bgp147","year":2009,"model":"Enzyme and human cancer-cell assays","summary":"MSP and KMSB are distinct HDAC-inhibitory metabolites; not dietary cancer-prevention evidence."}]},"sides":[{"conflict_id":"ee8136ef-7cee-57fa-b694-f001e0df604e","ordinal":0,"label":"Original preserved statement","revision_id":"1fa1ebde-141f-5d47-8a4f-ba87ff84a6c6","start_line":178,"end_line":178,"quote":"- Inhibits **HDACs** → chromatin opening, re-expression of silenced tumor suppressors","claim_id":null,"source_key":"molecular","source_title":"Selenium: the molecular cascade","claim_ids":[]},{"conflict_id":"ee8136ef-7cee-57fa-b694-f001e0df604e","ordinal":1,"label":"Original preserved statement","revision_id":"4cec6304-35d7-5560-9133-e6ea689db838","start_line":284,"end_line":284,"quote":"- **HDAC inhibition** → histone hyperacetylation → re-expression of silenced tumor suppressors (this is a bona fide epigenetic drug action)","claim_id":null,"source_key":"corrections","source_title":"Selenium corrections and deep dive","claim_ids":[]},{"conflict_id":"ee8136ef-7cee-57fa-b694-f001e0df604e","ordinal":2,"label":"Literature correction and experimental limits","revision_id":"80984e03-5f0f-5877-8094-afef7637444e","start_line":1683,"end_line":1688,"quote":"## HDAC effects need chemically distinct selenium metabolites\n\nMSP/KMSB inhibition evidence cannot be transferred to methylselenol or parent compounds as though they were the same species.\n\nKeep compound-specific claims; direct methylselenol HDAC inhibition is unestablished by these studies, not disproved in every context.\nPrimary reference: [α-Keto acid metabolites of organoselenium compounds inhibit histone deacetylase activity in human colon cancer cells](https://pmc.ncbi.nlm.nih.gov/articles/PMC2718078/)","claim_id":null,"source_key":"selenium-research-2026-09-17","source_title":"Selenium: literature corrections and mechanism additions","claim_ids":[]}]}],"research":{"topic":"Selenium scientific audit","plain_language":"This second distinct metabolite can also inhibit tested histone-deacetylase activity.","evidence_scope":"direct_experimental","papers":[{"key":"nian-2009","title":"α-Keto acid metabolites of organoselenium compounds inhibit histone deacetylase activity in human colon cancer cells","url":"https://pmc.ncbi.nlm.nih.gov/articles/PMC2718078/","doi":"10.1093/carcin/bgp147","year":2009,"model":"Enzyme and human cancer-cell assays","summary":"MSP and KMSB are distinct HDAC-inhibitory metabolites; not dietary cancer-prevention evidence."}]}}