| Literature DB >> 24681352 |
Vincenza Leone1, Concetta Langella1, Daniela D'Angelo1, Paula Mussnich1, Anne Wierinckx2, Luigi Terracciano3, Gerald Raverot4, Joel Lachuer5, Sandra Rotondi6, Marie-Lise Jaffrain-Rea7, Jacqueline Trouillas8, Alfredo Fusco9.
Abstract
MicroRNA (miRNA) deregulation plays a critical role in tumorigenesis. miR-23b and miR-130b are induced by thyrotropin in thyroid cells in a cAMP-dependent manner. The aim of our work has been to investigate the possible role of miR-23b and miR-130b in pituitary tumorigenesis. We have analyzed their expression in a panel of pituitary adenomas (PAs) including GH and NFPA adenomas. We report that miR-23b and miR-130b are drastically reduced in GH, gonadotroph and NFPA adenomas in comparison with normal pituitary gland. Interestingly, the overexpression of miR-23b and miR-130b inhibits cell proliferation arresting the cells in the G1 and G2 phase of the cell cycle, respectively. Moreover, we demonstrate that miR-23b and miR-130b target HMGA2 and cyclin A2 (CCNA2) genes, respectively. Finally, downregulation of miR-23b and miR-130b expression is associated with increased levels of their respective targets in human PAs. These findings suggest that miR-23b and miR-130b downregulation may contribute to pituitary tumorigenesis.Entities:
Keywords: CCNA2; HMGA2; Pituitary adenoma; microRNA
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Year: 2014 PMID： 24681352 DOI： 10.1016/j.mce.2014.03.002
Source DB: PubMed Journal: Mol Cell Endocrinol ISSN： 0303-7207 Impact factor: 4.102