title: Pituitary gene expression differs in D-galactose-induced cell senescence and steroid-induced prolactinomas.
abstract: In general, pituitary tumors are benign with low mitotic activity. Premature senescence has been considered to be a significant mechanism underlying this uniquely benign pituitary tumor. The present study aims to compare the expression of the associated proteins involved in premature senescence pathways among normal, aging and pituitary adenoma cells. We successfully induced the aging pituitary using continuous D‑galactose (D‑gal) injection as well as a prolactin‑secreting pituitary tumor via diethylstilbestrol implants. Compared with normal pituitary cells, the aging pituitary tissues revealed increased expression of IL‑6, C/EBPβ, p53, p21 and p16 and decreased expression of pituitary tumor transforming gene. In contrast, the expression of IL‑6, p21 and p16 was decreased in pituitary tumor cells compared with normal pituitary tissues. Taken together, multiple pathways including IL‑6/C/EBPβ, p53/p21 and p16 were activated in aging pituitary cells in response to D‑gal treatment. However, all these pathways were immune to pituitary tumors treated by chronic estrogen. The findings and the involvement of cytokines in a highly prevalent natural disease model (pituitary adenomas) indicate a potential use of this pathway as a target for effective therapy for tumor silencing and prevention of adenoma progression towards malignancy.
authors.affiliation: Department of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China.
authors.forename: Tiehui
authors.initials: T
authors.lastname: Zhang
authors.affiliation: Heilongjiang Key Laboratory of Anti‑Fibrosis Biotherapy, Mudanjiang Medical University, Mudanjiang, Heilongjiang 157011, P.R. China.
authors.forename: Binhai
authors.initials: B
authors.lastname: Zhao
authors.affiliation: Heilongjiang Key Laboratory of Anti‑Fibrosis Biotherapy, Mudanjiang Medical University, Mudanjiang, Heilongjiang 157011, P.R. China.
authors.forename: Jia
authors.initials: J
authors.lastname: Li
authors.affiliation: Heilongjiang Key Laboratory of Anti‑Fibrosis Biotherapy, Mudanjiang Medical University, Mudanjiang, Heilongjiang 157011, P.R. China.
authors.forename: Chunlei
authors.initials: C
authors.lastname: Zhang
authors.affiliation: Heilongjiang Key Laboratory of Anti‑Fibrosis Biotherapy, Mudanjiang Medical University, Mudanjiang, Heilongjiang 157011, P.R. China.
authors.forename: Hongzhi
authors.initials: H
authors.lastname: Li
authors.affiliation: Department of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China.
authors.forename: Jiang
authors.initials: J
authors.lastname: Wu
authors.affiliation: Department of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China.
authors.forename: Shiming
authors.initials: S
authors.lastname: Zhang
authors.affiliation: Department of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China.
authors.forename: Guozhen
authors.initials: G
authors.lastname: Hui
mesh_terms: D000367:Age Factors; D000818:Animals; D001835:Body Weight / Q000187:drug effects; D016922:Cellular Senescence / Q000187:drug effects* / Q000235:genetics*; D005690:Galactose / Q000494:pharmacology*; D015870:Gene Expression; D010902:Pituitary Gland / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D010911:Pituitary Neoplasms / Q000139:chemically induced / Q000235:genetics* / Q000378:metabolism; D015175:Prolactinoma / Q000139:chemically induced / Q000235:genetics* / Q000378:metabolism; D051381:Rats
chemical_list: D005690:Galactose