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FSH通过SATB1调控上皮性卵巢癌ES-2细胞的增殖和侵袭活性 被引量：2

Follicle Stimulatinghormone Controls Proliferation and Invasion Activity of Epithelial Ovarian Cancer ES-2 Cells by Specialat-Rich Sequence-Binding Protein 1
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摘要 目的:探讨特异AT序列结合蛋白1(specialAT-rich sequence-bindingprotein,SATB1)在卵泡刺激素(Follicle stimulating hormone,FSH)诱导的上皮性卵巢癌ES-2细胞增殖和侵袭中的作用。方法:以Real-time PCR检测不同浓度FSH(0、10、20、40、80mIU/ml)处理后SATB1基因mRNA表达水平的变化。实验分4组:①siCon组,转染si-阴性对照(si-Negative contro1)序列的实验组,对SATB1无干扰作用;②siSATB1组:转染特异性干扰下调SATB1的siSATB1序列;③FSH+siCon组:以FSH处理的siCon组;④FSH+siSATB1组:以FSH处理的siSATB1组。MTT法检测4组细胞的增殖情况,Western blotting技术检测4组细胞细胞周期蛋白(CyclinD1),基质金属蛋白酶2(MMP-2)的蛋白表达情况,Transwell侵袭实验检测4组细胞侵袭能力的变化。结果:1.FSH+siCon组的细胞增殖能力明显高于siCon组的细胞增殖能力,FSH+siCon组的Cyclin D1蛋白相对表达量0.90±0.08明显高于siCon组的0.37±0.01(P均<0.01),提示FSH具有促进ES-2细胞增殖的作用。2.FSH+siCon组的穿膜细胞数(302 12)个明显高于siCon组(139 19)个,FSH+siCon组的MMP-2蛋白相对表达量0.40±0.01明显高于siCon组的0.28±0.02,提示FSH具有促进ES-2细胞侵袭能力的作用。3.随着FSH浓度的增高,SATB1mRNA的表达量逐渐增加,分别为1,1.66±0.04,1.79±0.21,2.31±0.03,以FSH浓度为80mlU/ml时最显著(P<0.05)。4.FSH+siSATB1组的细胞增殖能力明显低于FSH+siCon组的细胞增殖能力,FSH+siSATB1组的Cyclin D1蛋白相对表达量0.22±0.02明显低于FSH+siCon组的0.90±0.08(P均<0.01);FSH+siSATB1组的穿膜细胞数(52 16)个低于FSH+siCon组的(302 12)个,FSH+siSATB1组的MMP-2蛋白相对表达量0.15±0.00明显低于FSH+siCon组的0.40±0.01(P均<0.01),FSH促进ES-2细胞增殖和侵袭的能力由于SATB1基因表达的下降而被阻断。结论:SATB1是FSH作用的重要靶分子,介导FSH对上皮性卵巢癌ES-2细胞系增殖、侵袭活性的调控。 Objective： To investigate the relationship between SATB1 （special AT-rich sequence-binding protein）and FSH （Follicle stimulating hormone ）,and their roles in regulating cell proliferation,invasion in epithelial ovarian carcinoma cells ES-2. Methods： Real-time PCR detects the expression levels of SATB1 in ES-2 cells after treatment with different concentrations of FSH （0,10,20,40,80mlU/ml）.ES-2 cells were divided into 4 groups：siCon group：transfected si-Negative control sequence which had no effect on SATB1 ;siSATB1 group：transfected siSATBl-specific sequence which down-regulated SATB1 ;FSH＋siCon group：siCon cells treated by FSH;FSH＋siSATB 1 ：siSATB 1 cells treated by FSH. MTT assay was used to determine cellular proliferative activity. Western blotting were used to determine the effect of FSH and SATB1 on the expression of cyclinD1 and MMP-2 in protein levels.The invasive activity was observed through matrigel invasion assay. Results： 1. The cell proliferation of FSH＋siCon was higher than that of siCon.The protein expression of Cyclin D 1 in FSH＋siCon was higher than that in siCon. （ P〈0.01）.It showed that FSH induced cell proliferation of ES-2.2. The numbers of ES-2 that penetrated the basement menbrane in FSH＋siCon were more than that in siCon. The protein expression of MMP-2 in FSH＋siCon was higher than that in siCon. （ P〈0.01）.It suggested that FSH induced cell invasion of ES-2.3.The expression of SATB1 increased as increasing in the concentration of FSH,the results were： 1,1.66±0.04, 1.79± 0.21,2.31 ± 0.03 （P〈0.05）. FSH up-regulated the expression of SATB1 in a dose-dependent manner.4. The cell proliferation in FSH＋siSATB1 was lower than that in FSH＋siCon.The protein expression of Cyclin D1 in FSH＋siSATB1 was lower than that in FSH＋siCon. （ P〈0.01）,the same as in cell invasion. Inhibition of SATB1 by RNA interference blocked the proliferation and invasion of ES-2 induced by FSH.Conelusions： FSH regulates cell proliferation and invasion by SATB 1 gene.
作者 冯怡雯 魏桠楠 祝颖 周冬梅 吴凌 杨婷 席晓薇 张箴波 丰有吉
机构地区 上海交通大学附属上海第一人民医院妇产科
出处 《现代生物医学进展》 CAS 2011年第15期2801-2805,共5页 Progress in Modern Biomedicine
基金 国家自然科学基金(编号:81001155和81020108027) 上海市卫生局面上项目(编号:2009028)
关键词 上皮性卵巢癌 SATB1 FSH SIRNA Epithelial Ovarian Carcinoma FSH SATB1 siRNA
分类号 R737.33 [医药卫生—肿瘤]
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参考文献12

  • 1Sicinski P, Donaher JL, Geng Y, et al. Cyclin D2 is an FSH-responsive gene involved in gonadal cell proiferation and oncogenesis [J].Nature, 1996,384(6608):470-474.
  • 2Alam H, Maizels ET, Park Y, et al. Follicle-stimulating hormone activation of hypoxia-inducible factor-1 by the phosphatidylinositol 3-kinase/AKT/Ras homolog enriched in brain (Rheb)/mammalian target of rapamycin (mTOR) pathway is necessary for induction of select protein markers of follicular differentiation [J]. J Biol Chem, 2004, 279(19): 19431 - 19440.
  • 3Meroni SB, Riera MF, Pellizzari EH, et al. FSH activates phosphatidy- linositol 3-kinase/protein kinase B signaling pathway in 20-day-old Sertoli cells independently of IGF-I [J].J Endocrinol, 2004, 180 (2): 257-265.
  • 4Choi JH, Choi KC, Auersperg N, et al. Gonadotropins upregulate the epidermal growth factor receptor through activation of mitogen-acti- vated protein kinases and phosphatidyl-inositol-3-kinase in human ovarian surface epithelial cells [J].Endocr Relat Cancer,2005, 12(2): 407-421.
  • 5Syed V, Ulinski G, Mok SC, et al. Reproductive hormone-induced,STAT3-mediated interleukin 6 action in normal and malignant hman ovarian surface epithelial cell [J].J Natl Cancer Inst,2002,94 (8): 617-629.
  • 6Purbey PK, Singh S, Kumar PP, et al. PDZ domain-mediated dimeriza- tion and homeodomain-directed specificity are required for high-affini- ty DNA binding by SATB1 [J].Nucleic Acids Res, 2008, 36 (7): 2107-2122.
  • 7Purbey PK, Singh S, Notani D, et al. Acetylation-dependent interaction of SATB1 and CtBP1 mediates transcriptional repression by SATB1 [J]. Mol Cell Biol, 2009, 29(5):1321-1337.
  • 8Seo J, Lozano MM, Dudley JP. Nuclear matrix binding regulates SATBl-mediated transcriptional repression [.1]. J Biol Chem, 2005, 280(26):24600-24609.
  • 9Cai S, Han H J, Kohwi-Shigematsu T. Tissue-specific nuclear architect- ure and gene expression regulated by SATB1 [J]. Nat Genet, 2003,34 (1):42-51.
  • 10Alvarez JD, Yasui D H, Niida H, et al. The MAR-binding protein SATB 1 orchestrates temporal and spatial expression of multiplegene- s during T-cell development [J].Genes Dev, 2000, 14(5):521-535.

二级参考文献12

  • 1Jemal A, Siegel R, Ward E, et al. Cancer Statistics, 2009 [J]. CA Cancer J Clin,2009, 59(4):225-249.
  • 2Dickinson LA, Joh T, Kohwi Y, et al. A tissue-specific MAR/SAR i DNA-binding protein with unusual binding site recognition [J].Cell, 1992,70(4):631-645.
  • 3Purbey PK, .Singh S, Kumar PP, et al. PDZ domain-mediated dimerization and homeodomain-directed specificity are required for high-affinity DNA binding by SATB 1 [J].Nucleic Acids Res, 2008, 36 (7): 2107-2122.
  • 4Purbey PK, Singh S, Notani D, et al. Acetylation-dependent interaction of SATB 1 and CtBP 1 mediates transcriptional repression by SATB 1 [J]. Mol Cell Biol, 2009, 29(5): 1321-1337.
  • 5Seo J, Lozano MM, Dudley JP. Nuclear matrix binding regulates SATBl-mediated transcriptional repression [J]. J Biol Chem, 2005, 280(26):24600-24609.
  • 6Cai S, Han HJ, Kohwi-Shigematsu T. Tissue-specific nuclear architecture and gene expression regulated by SATB1 [J]. Nat Genet, 2003,34 (1):42-51.
  • 7Alvarez JD, Yasui D H, Niida H, et al. The ,MAR-binding protein SATB 1 orchestrates temporal and spatial expression of multiplegenes during T-cell development [J].Genes Dev, 2000, 14(5):521-535.
  • 8Nie H, Yao X, Maika SD, et al. SATB1 is required for CD8 coreceptor reversal[J]. Mol Immunol, 2008, 46(1): 207-211.
  • 9Cai S, Lee CC, Kohwi-Shigematsu T. SATB1 packages densely looped, transcriptionally active chromatin for coordinated expression of cytokine genes[J].Nat Genet,2006,38( 11): 1278-1288.
  • 10Zhang J, Ma C, Han X, et al. The bcl-2 major breakpoint region (mbr) . possesses transcriptional regulatory function [J].Gene, 2006,379(9): 127-131.

共引文献3

同被引文献22

  • 1宋光辉,刘惜时.卵泡刺激素对上皮性卵巢癌细胞株的增殖及E-钙粘素表达的影响[J].实用妇产科杂志,2004,20(5):294-297. 被引量：4
  • 2曾泽毅.中华妇产科学[M].北京:人民卫生出版社, 1999.2 313.
  • 3Aoyama Y,Yamamoto Y,Yamaguchi F,Kitajima Y.Low to high Ca2+-switch causes phosphorylation and association of desmocollin 3 with plakoglobin and desmoglein 3 in cultured keratinocytes[J].Exp Derma-tol,2009,18:404-408.
  • 4Cui T,Chen Y,Yang L,Knosel T,ZNler K,Huber O,et al.DSC3 expression is regulated by p53,and methyl ation of DSC3 DNA is a prognostic marker in human colorectal cancer[J].Br J Cancer,2011,104:1013-1019.
  • 5Chen J,O' Shea C,Fitzpatrick J E,Koster M I,Koch P J.Loss of desmocollin 3 in skin tumor development and progression[J].Mol Carcinog,2012,51:535-545.
  • 6Wang L,Liu T,Wang Y,Cao L,Nishioka M,Aguirre R L,et al.Altered expression of desmocollin 3,desmo glein 3,and β-catenin in oral squamous cell carcinoma:correlation with lymph node metastasis and cell prolif-eration[J].Virchows Arch,2007,451:959-966.
  • 7Hamidov Z,Altendorf-Hofmann A,Chen Y,Settmacher U,Petersen I,Knosel T.Reduced expression of desmo-collin 2 is an independent prognostic biomarker for shorter patients survival in pancreatic ductal adenocar-cinoma[J].J Clin Pathol,2011,64:990-994.
  • 8Monica V,Ceppi P,Righi L,Tavaglione V,Volante M,Pelosi G,et al.Desmocollin-3:a new marker of squamous differentiation in undifferentiated large-cell carcinoma of the lung[J].Mod Pathol,2009,22:709-717.
  • 9Kolegraff K,Nava P,Helms M N,Parkos C A,Nus-rat A.Loss of desmocollin-2 confers a tumorigenic phe-notype to colonic epithelial cells through activation of Akt/β-catenin signaling[J].Mol Biol Cell,2011,22:1121-1134.
  • 10Remmele W,Stegner H E.[Recommendation for uni-form definition of an immunoreactive score(IRS)for immunohistochemical estrogen receptor detection(ER-ICA)in breast cancer tissue][J].Pathologe,1987,8:138-140.

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现代生物医学进展
2011年 第15期

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