Loss of 15-hydroxyprostaglandin dehydrogenase indicates a tumor suppressor role in pituitary adenomas
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Updated: May 22, 2026
Endoscopic Endonasal Trans-sphenoidal Approach: Minimally Invasive Surgery for Pituitary Adenomas
Published on: January 17, 2018
Ji-Wei Bai1, Zhe Wang, Song-Bai Gui
1Beijing Neurosurgical Institute, Capital Medical University, and Neurosurgical Department, Beijing Tiantan Hospital, Dongcheng District, Beijing 100050, PR China.
Abstract:
15-hydroxyprostaglandin dehydrogenase (15-PGDH) may function as a tumor suppressor that antagonizes the action of the cyclooxygenase-2 (COX-2) oncogene in several types of tumors. However, it is unknown if it has a role in the pituitary. Recently, our group found that 15-PGDH expression was low in prolactin (PRL) secreting adenomas (prolactinomas) and growth hormone (GH) secreting adenomas (GHomas) using fiber-optic BeadArray technology. In this study, we examined the relative expression of 15-PGDH and COX-2 mRNA in clinical specimens and examined the effects of 15-PGDH on GH3 rat pituitary tumor cell proliferation, apoptosis and hormone secretion. 15-PGDH expression was lower and COX-2 expression was higher in prolactinomas and GHomas compared with normal controls. Overexpressed 15-PGDH inhibited tumor cell proliferation and induced apoptosis. It had a significant suppressive effect on mRNA levels and on the secretion of PRL and GH in GH3 cells. The inhibition of cell proliferation was accompanied by the decreased expression of cox-2, matrix metalloproteinase-9 (MMP-9) and B cell leukemia/lymphoma-2 (Bcl-2). These data are suggestive of a previously unrecognized pathway in pituitary tumorigenesis, and this novel observation may shed light on therapeutic strategies for pituitary tumors.
Insights
15-hydroxyprostaglandin dehydrogenase (15-PGDH) acts as a tumor suppressor in pituitary tumors. Lower 15-PGDH and higher cyclooxygenase-2 (COX-2) expression correlate with prolactinomas and GHomas, suggesting a new therapeutic target.
Area of Science:
- Endocrinology
- Oncology
- Molecular Biology
Background:
- 15-hydroxyprostaglandin dehydrogenase (15-PGDH) is a potential tumor suppressor.
- Its role in pituitary tumors, specifically prolactinomas and GHomas, is not well understood.
- Previous studies indicated low 15-PGDH expression in these pituitary adenomas.
Purpose of the Study:
- To investigate the expression of 15-PGDH and cyclooxygenase-2 (COX-2) in pituitary tumors.
- To determine the functional role of 15-PGDH in pituitary tumor cell behavior, including proliferation, apoptosis, and hormone secretion.
- To explore the potential of 15-PGDH as a therapeutic target for pituitary tumors.
Main Methods:
- Analysis of 15-PGDH and COX-2 mRNA expression in clinical pituitary tumor specimens and normal controls.
- Overexpression of 15-PGDH in GH3 rat pituitary tumor cells.
- Assessment of cell proliferation, apoptosis, and secretion of prolactin (PRL) and growth hormone (GH) in GH3 cells.
- Measurement of key gene expressions including COX-2, MMP-9, and Bcl-2.
Main Results:
- 15-PGDH expression was significantly lower, while COX-2 expression was higher in prolactinomas and GHomas compared to normal pituitary tissue.
- Overexpression of 15-PGDH inhibited GH3 cell proliferation and induced apoptosis.
- 15-PGDH overexpression suppressed both mRNA levels and secretion of PRL and GH.
- Inhibition of proliferation was associated with decreased expression of COX-2, MMP-9, and Bcl-2.
Conclusions:
- 15-PGDH acts as a tumor suppressor in pituitary tumors, antagonizing COX-2.
- Altered 15-PGDH and COX-2 expression represents a novel pathway in pituitary tumorigenesis.
- Modulating 15-PGDH activity may offer a new therapeutic strategy for pituitary tumors.
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