Chile T.,Laboratory for Cellular and Molecular Endocrinology LIM 25 |
Correa-Giannella M.L.,Laboratory for Cellular and Molecular Endocrinology LIM 25 |
Fortes M.A.H.Z.,Laboratory for Cellular and Molecular Endocrinology LIM 25 |
Bronstein M.D.,Neuroendocrine Unit |
And 3 more authors.
Journal of Endocrinological Investigation
Background: Pituitary tumors account for approximately 10-15% of intracranial neoplasms. Aim: Using the cDNA microarray method, we have previously compared expression under two distinct conditions: a pool of 4 clinically non-functioning pituitary adenomas (NFPA) and a spinal cord metastasis of a non-functioning pituitary carcinoma, in order to gain biological insights into genomic changes of pituitary neoplasias. In the present study, we further investigated the mRNA expression of 3 selected genes previously described as being involved in other neoplasias based on a series of 60 pituitary adenomas: CRABP1 (cellular retinoic acid binding protein 1), GRP (gastrin-releasing peptide), and RERG (Ras-related, estrogen-regulated, growth inhibitor). Material and methods: The expression of CRABP1, GRP, and RERG was determined by quantitative RT-PCR. Results: A significantly higher content of CRABP1 mRNA was observed in NFPA compared to functioning adenomas, and PRL-secreting adenomas showed a lower expression of this gene compared to normal pituitary. A lower expression of GRP mRNA was detected in NFPA compared to normal pituitary and also to functioning adenomas. RERG mRNA was overexpressed in NFPA in comparison to functioning adenomas and to normal pituitary. Among the functioning adenomas, only the ACTH-secreting adenomas presented a higher expression of RERG mRNA compared to normal pituitary. Conclusions: The findings of differential expression of CRABP1 in prolactinomas and of RERG in NFPA compared to normal pituitary suggests that retinoic acid and estrogen receptor, respectively, could be involved in the tumorigenesis of these adenomas subtypes. Additional studies are required to further confirm this hypothesis. ©2011, Editrice Kurtis. Source