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Published on: September 1, 2015
Protein Kinase C Delta restrains growth in ACTH-secreting pituitary adenoma cells
Erica Gentilin1, Carmelina Di Pasquale2, Teresa Gagliano2
1Section of Endocrinology & Internal Medicine, Dept. of Medical Sciences, University of Ferrara, Italy; Laboratorio in rete del Tecnopolo "Tecnologie delle terapie avanzate" (LTTA) of the University of Ferrara, Italy.
Abstract:
Protein Kinase C Delta (PRKCD) has been highlighted among disrupted pathways in corticotroph adenomas. PRKCD is expressed at low level in human corticotroph adenomas and controls cell cycle in vitro. Therefore, PRKCD may play an important role in the development/progression of corticotroph adenomas, warranting further studies to understand the role of PRKCD and related pathways in restraining pituitary cell growth. We evaluated PRKCD role in influencing cell behavior in terms of cell viability, hormone expression and protein expression profile, by silencing PRKCD in AtT-20/D16v-F2 cells. PRKCD silencing increases cell viability, enhances hormone expression and induces morphological changes associated with deregulation of adhesion molecules. PRKCD silencing is associated with an increase in Epithelial Growth Factor Receptor (EGFR) expression, a marker of tumor aggressive behavior, and sensitivity to anti-EGFR molecules. PRKCD might restrain corticotroph adenoma cells from acquiring an aggressive behavior, candidating PRKCD as a possible molecular target for the treatment of corticotroph adenomas.
Insights
Protein Kinase C Delta (PRKCD) restrains pituitary tumor growth. Silencing PRKCD in corticotroph adenomas increases cell viability and aggressiveness, suggesting PRKCD as a potential therapeutic target.
Area of Science:
- Endocrinology
- Molecular Biology
- Oncology
Background:
- Protein Kinase C Delta (PRKCD) is implicated in disrupted pathways within corticotroph adenomas.
- Low PRKCD expression in human corticotroph adenomas suggests a role in cell cycle control.
- Further research is needed to understand PRKCD's function in pituitary cell growth regulation.
Purpose of the Study:
- To investigate the role of PRKCD in modulating corticotroph adenoma cell behavior.
- To assess the impact of PRKCD silencing on cell viability, hormone expression, and protein profiles.
- To determine if PRKCD influences aggressive tumor characteristics.
Main Methods:
- PRKCD was silenced in AtT-20/D16v-F2 corticotroph adenoma cells.
- Cell viability, hormone expression, and protein expression were analyzed.
- Changes in cell morphology and adhesion molecule expression were evaluated.
Main Results:
- PRKCD silencing led to increased cell viability and enhanced hormone expression.
- Morphological changes indicated deregulation of adhesion molecules.
- Epithelial Growth Factor Receptor (EGFR) expression increased, correlating with aggressive behavior and sensitivity to anti-EGFR therapies.
Conclusions:
- PRKCD appears to inhibit aggressive behavior in corticotroph adenoma cells.
- PRKCD warrants further investigation as a potential molecular target for corticotroph adenoma treatment.
- Targeting PRKCD may offer a novel therapeutic strategy for pituitary tumors.
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