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Updated: May 1, 2026

miRNA Expression Analyses in Prostate Cancer Clinical Tissues
Published on: September 8, 2015
Mir-23b and miR-130b expression is downregulated in pituitary adenomas
Vincenza Leone1, Concetta Langella1, Daniela D'Angelo1
1Istituto di Endocrinologia ed Oncologia Sperimentale del CNR, c/o Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Scuola di Medicina e Chirurgia di Napoli, Università degli Studi di Napoli "Federico II", Naples, Italy.
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.
Insights
Reduced microRNAs (miRNAs), specifically miR-23b and miR-130b, are linked to pituitary adenomas. Their downregulation may promote tumor growth by increasing target genes like HMGA2 and CCNA2.
Area of Science:
- Endocrinology
- Molecular Biology
- Oncology
Background:
- MicroRNA (miRNA) deregulation is implicated in tumorigenesis.
- Thyrotropin induces miR-23b and miR-130b in thyroid cells via cAMP.
- The role of these miRNAs in pituitary tumorigenesis requires investigation.
Purpose of the Study:
- To investigate the role of miR-23b and miR-130b in pituitary adenomas (PAs).
- To analyze the expression levels of miR-23b and miR-130b in various PAs.
- To determine the functional impact of miR-23b and miR-130b on pituitary cell proliferation and their target genes.
Main Methods:
- Analysis of miR-23b and miR-130b expression in human pituitary adenomas (GH and NFPA) and normal pituitary tissue.
- Overexpression studies to assess the effect of miR-23b and miR-130b on cell proliferation and cell cycle progression.
- Identification of target genes for miR-23b and miR-130b using molecular techniques.
Main Results:
- miR-23b and miR-130b expression are significantly reduced in GH, gonadotroph, and NFPA adenomas compared to normal pituitary tissue.
- Overexpression of miR-23b inhibits cell proliferation by arresting cells in G1 phase.
- Overexpression of miR-130b inhibits cell proliferation by arresting cells in G2 phase.
- miR-23b targets HMGA2, and miR-130b targets cyclin A2 (CCNA2).
- Downregulation of these miRNAs correlates with increased levels of their target genes in PAs.
Conclusions:
- Downregulation of miR-23b and miR-130b is a common feature in pituitary adenomas.
- These miRNAs act as tumor suppressors by inhibiting cell proliferation.
- The reduced expression of miR-23b and miR-130b, leading to increased target gene levels, may contribute to pituitary tumorigenesis.
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