ArticleJournal of cellular and molecular medicine2019
TSP-1 is downregulated and inversely correlates with miR-449c expression in Cushing's disease.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- The role of methylation in pituitary neuroendocrine tumors current insights and emerging perspectives.Molecular biology reports · 2026Review
- Cushing's Disease in the Animal Kingdom: Translational Insights for Human Medicine.International journal of molecular sciences · 2025Review
- Current understanding of the role of DNA methylation in pituitary neuroendocrine tumors.Neuro-oncology advances · 2025Article
- Liquid Biopsy in Pituitary Neuroendocrine Tumors-Potential Biomarkers for Diagnosis, Prognosis, and Therapy.International journal of molecular sciences · 2025Review
- Diagnostic and prognostic utility of plasma thrombospondin-1 levels in traumatic brain injury.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2024Article
- Scleral remodeling during myopia development in mice eyes: a potential role of thrombospondin-1.Molecular medicine (Cambridge, Mass.) · 2024Article
- Astrocyte: A Foe or a Friend in Intellectual Disability-Related Diseases.Frontiers in synaptic neuroscience · 2022Review
- Wnt-Signaling Regulated by Glucocorticoid-Induced miRNAs.International journal of molecular sciences · 2021Article
- MicroRNAs as Potential Biomarkers in Pituitary Adenomas.Non-coding RNA · 2021Review
- Novel Insights into Pituitary Tumorigenesis: Genetic and Epigenetic Mechanisms.Endocrine reviews · 2020Review
- Genetic and Epigenetic Causes of Pituitary Adenomas.Frontiers in endocrinology · 2020Review
- Gastric Cancer Cell-Derived Exosomal microRNA-23a Promotes Angiogenesis by Targeting PTEN.Frontiers in oncology · 2020Article
- TSP-1 is downregulated and inversely correlates with miR-449c expression in Cushing's disease.Journal of cellular and molecular medicine · 2019Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenesis of Cushing's disease, which is caused by pituitary corticotroph adenoma, remains to be studied. Secreted angioinhibitory factor thrombospondin-1 (TSP-1) is an adhesive glycoprotein that mediates cell-to-cell and cell-to-matrix interactions and is associated with platelet aggregation, angiogenesis and tumorigenesis. We have found that the expression of TSP-1 is significantly lower in human pituitary corticotroph tumours compared with normal adenohypophysis. This study aims to elucidate the role of TSP-1 in regulating the tumour function of pituitary adenomas. Forced overexpression of TSP-1 in a murine AtT20 pituitary corticotroph tumour cell line decreased corticotroph precursor hormone proopiomelanocortin (POMC) transcription and adrenocorticotropic hormone (ACTH) secretion. Functional studies showed that TSP-1 overexpression in pituitary adenoma cells suppressed proliferation, migration and invasion. We have demonstrated that TSP-1 is a direct target of miR-449c. Further study showed that miR-449c activity enhanced tumorigenesis by directly inhibiting TSP-1 expression. Low expression of lncTHBS1, along with low expression of TSP-1, was associated with the high expression of miR-449c in Cushing's disease patients. Furthermore, RNA-immunoprecipitation associates miR-449c with lncTHBS1 suggesting that lncTHBS1 might be a negative regulator of miR-449c. Taken together, this study has demonstrated that lncTHBS1 might function as competing endogenous RNA for miR-449c, which could suppress the development of Cushing's disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.