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CEBPD抑制催乳素表达和催乳素瘤细胞增殖。

CEBPD suppresses prolactin expression and prolactinoma cell proliferation.

作者信息

Tong Yunguang, Zhou Jin, Mizutani Jun, Fukuoka Hidenori, Ren Song-Guang, Gutierrez-Hartmann Arthur, Koeffler H Phillip, Melmed Shlomo

机构信息

Academic Affairs, Los Angeles, California 90048, USA.

出版信息

Mol Endocrinol. 2011 Nov;25(11):1880-91. doi: 10.1210/me.2011-1075. Epub 2011 Oct 6.

Abstract

Hyperprolactinemia, usually caused by a pituitary lactotroph tumor, leads to galactorrhea and infertility. Increased prolactin (PRL) levels may be due to enhanced PRL expression or proliferation of PRL-secreting cells. We hypothesize that PRL expression and PRL-secreting cell proliferation are linked. Using microarray-based gene expression profiling, we identified CCAAT-enhancer-binding protein δ (CEBPD) transcription factor as a critical gene that regulates both PRL expression and lactotroph cell proliferation. CEBPD expression levels are decreased approximately 7-fold in experimental rat prolactinoma cells. Forced expression of this transcription factor in PRL-secreting cells (GH3 and MMQ) inhibited PRL expression and cellular proliferation, and CEBPD knockdown by small interfering RNA leads to increased PRL expression in both cell lines. To determine mechanisms underlying this observation, we determined binding of CEBPD to the PRL promoter and also showed marked suppression (96%) of PRL promoter activity. CEBPD and Pit1 interact and attenuate each other's binding to the PRL promoter. CEBPD also suppresses expression of proliferation-related genes, including c-Myc, survivin, as well as cyclins B1, B2, and D1. These results show that PRL expression and cell proliferation are controlled in part by CEBPD.

摘要

高催乳素血症通常由垂体催乳素细胞肿瘤引起,可导致溢乳和不孕。催乳素(PRL)水平升高可能是由于PRL表达增强或PRL分泌细胞增殖所致。我们推测PRL表达与PRL分泌细胞增殖有关。通过基于微阵列的基因表达谱分析,我们确定CCAAT增强子结合蛋白δ(CEBPD)转录因子是调节PRL表达和催乳素细胞增殖的关键基因。在实验性大鼠催乳素瘤细胞中,CEBPD表达水平降低了约7倍。在PRL分泌细胞(GH3和MMQ)中强制表达该转录因子可抑制PRL表达和细胞增殖,而小干扰RNA介导的CEBPD敲低则导致这两种细胞系中PRL表达增加。为了确定这一观察结果的潜在机制,我们检测了CEBPD与PRL启动子的结合情况,并发现PRL启动子活性受到显著抑制(96%)。CEBPD与Pit1相互作用并减弱彼此与PRL启动子的结合。CEBPD还抑制包括c-Myc、survivin以及细胞周期蛋白B1、B2和D1在内的增殖相关基因的表达。这些结果表明,PRL表达和细胞增殖部分受CEBPD调控。

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