title: Loss of 15-hydroxyprostaglandin dehydrogenase indicates a tumor suppressor             role in pituitary adenomas.
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.
authors.affiliation: Beijing Neurosurgical Institute, Capital Medical University, and Neurosurgical Department, Beijing Tiantan Hospital, Dongcheng District, Beijing 100050, PR China.
authors.forename: Ji-Wei
authors.initials: JW
authors.lastname: Bai
authors.forename: Zhe
authors.initials: Z
authors.lastname: Wang
authors.forename: Song-Bai
authors.initials: SB
authors.lastname: Gui
authors.forename: Ya-Zhuo
authors.initials: YZ
authors.lastname: Zhang
mesh_terms: D000328:Adult; D000818:Animals; D017209:Apoptosis / Q000502:physiology; D048708:Cell Growth Processes / Q000502:physiology; D045744:Cell Line, Tumor; D051546:Cyclooxygenase 2 / Q000096:biosynthesis / Q000235:genetics; D015232:Dinoprostone / Q000378:metabolism; D005260:Female; D016147:Genes, Tumor Suppressor; D013006:Growth Hormone / Q000378:metabolism; D049912:Growth Hormone-Secreting Pituitary Adenoma / Q000201:enzymology* / Q000235:genetics / Q000473:pathology; D006801:Humans; D006911:Hydroxyprostaglandin Dehydrogenases / Q000096:biosynthesis / Q000172:deficiency* / Q000235:genetics; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D010911:Pituitary Neoplasms / Q000201:enzymology* / Q000235:genetics / Q000473:pathology; D011388:Prolactin / Q000378:metabolism; D015175:Prolactinoma / Q000201:enzymology* / Q000235:genetics / Q000473:pathology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D051381:Rats; D014162:Transfection; D055815:Young Adult
chemical_list: D019253:Proto-Oncogene Proteins c-bcl-2; D012333:RNA, Messenger; D011388:Prolactin; D013006:Growth Hormone; D006911:Hydroxyprostaglandin Dehydrogenases; C035859:15-hydroxyprostaglandin dehydrogenase; D051546:Cyclooxygenase 2; D020780:Matrix Metalloproteinase 9; D015232:Dinoprostone