ArticleNeuroendocrinology2023
Silibinin, an HSP90 Inhibitor, on Human ACTH-Secreting Adenomas.
Article in Neuroendocrinology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 16 citations in OpenAlex.
- Silibinin mitigates AKI-to-CKD transition via MAPK and PI3K/AKT signaling pathways in Ischemia-Reperfusion injury.Scientific reports · 2025Article
- Review
- New Trends in Treating Cushing's Disease.TouchREVIEWS in endocrinology · 2024Article
- Gut microbiota composition and metabolic characteristics in patients with Craniopharyngioma.BMC cancer · 2024Article
- Current and Emerging Pharmacological Therapies for Cushing's Disease.Current pharmaceutical design · 2024Review
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThe glucocorticoid receptor is pivotal to control corticotrophin (ACTH) secretion, and its function is closely linked to the heat shock protein 90 (HSP90) chaperone complex. Impaired sensitivity to glucocorticoid feedback is a hallmark of human corticotroph adenomas, i.e., Cushing's disease, a disorder with few medical treatment options. Silibinin, a HSP90 inhibitor, has been studied in tumoral corticotroph cells and its use proposed in Cushing's disease. Aim of the present study was to further investigate the effect of silibinin on human corticotroph adenomas in vitro.
methodsSeven human ACTH-secreting pituitary adenomas were established in culture and treated with 10-50 µ<sc>m</sc> silibinin with/without dexamethasone for up to 72 h. ACTH medium levels were measured, and POMC and glucocorticoid receptor, i.e., NR3C1, gene expression assessed.
resultsSilibinin reduced spontaneous ACTH secretion and restored sensitivity to steroid negative feedback to a different extent in individual adenomas. POMC expression was decreased in both control and dexamethasone-treated wells in specimens sensitive to silibinin. Interestingly, silibinin reduced constitutive NR3C1 expression and reversed the dexamethasone-induced inhibition.
conclusionsOur findings indicate that silibinin can inhibit ACTH synthesis and secretion in individual human corticotroph adenomas and directly affects NR3C1 gene expression. These results reveal promising effects of this HSP90 inhibitor on human corticotroph adenomas and support an innovative target treatment for patients with Cushing's disease.
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