期刊文献+

6种microRNAs在前列腺癌组织中的表达 被引量:16

Expressions of 6 microRNAs in prostate cancer
原文传递
导出
摘要 目的:研究表明miRNAs在人类恶性肿瘤的发生发展过程中起着重要作用,本研究检测6种miRNAs:miR-98、let-7d、let-7g、miR-96、miR-182及miR-183在前列腺癌组织中的表达情况及其临床意义。方法:采用原位分子杂交方法,结合组织芯片技术分别检测38例BPH和52例前列腺癌中6种miRNAs的表达情况。并对前列腺癌组织中6种miRNA与Gleason评分,临床分期及6种miRNA间进行相关分析。结果:6种miRNAs中,与BPH组织相比,在前列腺癌组织中表达降低的为miR-98、let-7d、let-7g;而表达升高的为miR-96、miR-182及miR-183,差异均有统计学意义(P<0.05)。6种miRNAs的表达与前列腺癌的Gleason评分均相关(P<0.05),但与患者的年龄及血清PSA水平均无明显相关性(P>0.05)。其中miR-96和miR-182的表达与前列腺癌的临床分期均有相关性(P<0.05),miR-98和miR-96的表达均与肿瘤累及前列腺的叶数存在相关性(P<0.05)。另外,前列腺癌组织中,miR-96、miR-182及miR-183的表达彼此之间呈正相关(P<0.01,r分别为0.41,0.44),let-7d与let-7g的表达之间呈正相关(P<0.01,r=0.46),miR-98与let-7d及let-7g的表达之间呈正相关(P<0.05,r分别为0.31,0.34)。结论:miR-98、let-7d、let-7g、miR-96、miR-182及miR-183构成的miRNA表达谱在一定程度上反映了前列腺癌的生物学行为,可能作为前列腺癌早期诊断和预后评估的重要生物标记物。 Objective: Experimental evidence shows that microRNAs play an important role in the initiation and progression of human malignancies. The present study aimed to investigate the expressions of 6 microRNAs in prostate cancer (PCa) and their clinical significance. Methods: We investigated the expression profiles of 6 microRNAs (let-7g, let-7d, miR-98, miR-96, miR-182 and miR-183 ) using the method of locked nucleic acid (LNA)-modified oligonueleotide in situ hybridization (ISH) and the technology of tissue mieroarray (TMA) with the formalin-fixed paraffin-embedded (FFPE) specimens from 52 patients with PCa and 38 with benign prostatic hyperplasia (BPH). Then we analyzed the correlation among the expressions of the 6 microRNAs in PCa and their correlation with the Gleason score and clinical stages of PCa. Results : Compared with BPH, the PCa patients showed decreased expressions of miR-98, let-7d and let-7g, and decreased expressions of miR-96, miR-182 and miR-183, with statistically significant differences between the two groups ( P 〈 0.05 ). The positive rate of the 6 microRNAs was significantly correlated with the Gleason grades of PCa (P 〈0.05) , but not with the age and serum PSA concentration of the patients (P 〉0.05). The expressions of miR-96 and miR-182 were correlated with the clinical stages of the tumor ( P 〈 0.05 ). There was a positive correlation among the expressions of miR-96, miR-182 and miR-183 ( P = 0.00, r = 0.41 ), as well as between the expressions of let-7d and let-7g ( P = 0.00, r = 0.46) in the PCa tissues. And the expression of miR-98 was positively correlated with those of let-7d and let-7g (P = 0.00, r = 0.46). Conclusion: The expression profiles of the microRNAs let-7d, let-7g, miR-98, miR-96, miR-182 and miR-183 reflect the biological behavior of PCa to some extent, and might be important biomarkers for the early detection and prognostic assessment of prostate cancer. Nat/ J Androl, 2010, 16 (7): 599-605
出处 《中华男科学杂志》 CAS CSCD 北大核心 2010年第7期599-605,共7页 National Journal of Andrology
关键词 微小RNA 前列腺癌 良性前列腺增生 组织芯片 原位分子杂交 microRNA prostate cancer benign prostatic hyperplasia tissue microarray in situ hybridization
  • 相关文献

参考文献11

  • 1高丽芳,徐德启,邵月婷,赵丹,赵雪俭.RNA干扰技术沉默STAT3对人前列腺癌细胞生长的抑制作用[J].中华男科学杂志,2005,11(1):29-33. 被引量:17
  • 2Gregory RI, Shiekhattar R. MicroRNA biogenesis and cancer. Cancer Res, 2005, 65(9) : 3509-3512.
  • 3Mendell JT. MicroRNAs : Critical regulators of development, cellular physiology and malignancy. Cell Cycle, 2005, 4 (9): 1179-1184.
  • 4Calin GA, Sevignani C, Dumitru CD, et al. Human microRNA genes are frequently located at fragile sites and genomic regions involved in cancers. Proc Natl Acad Sci USA, 2004, 101 ( 9 ) : 2999-3004.
  • 5Lu J, Getz G, Miska EA, et al. MicroRNA expression profiles classify human cancers. Nature, 2005, 435 (7043) : 834-838.
  • 6Liu CG, Calin GA, Meloon B, et al. An oligonucleotide micro- chip for genome-wide microRNA profiling in human and mouse tissues. Proc Natl Acad Sci USA, 2004, 101 (26) : 9740-9744.
  • 7Porkka KP, Pfeiffer MJ, Wahefing KK, et al. MieroRNA expression profiling in prostate cancer. Cancer Res, 2007, 67 (13) : 6130-6135.
  • 8Johnson SM, Grosshans H, Shingara J, et al. RAS is regulated by the let-7 microRNA family. Cell, 2005, 120(5) : 635-647.
  • 9Peter ME. Let-7 and miR-200 microRNAs: Guardians against pluripotency and cancer progression. Cell Cycle, 2009, 8 ( 6 ) : 843- 852.
  • 10Ozen M, Creighton C J, Ozdemir M, et al. Widespread deregulation of microRNA expression in human prostate cancer. Oncogene, 2008 ; 27(12) : 1788-1793.

二级参考文献13

  • 1Weiss JM, Nath A, Major EO, et al. HIV-1 Tat induces monocyte chemoattractant protein-l-mediated monocyte transmigration across a model of the human blood-brain barrier and up-regulates CCR5 expression on human monocytes[ J]. J Immunol, 1999,163 ( 5 ) :2953-2959.
  • 2Bowman T, Garcia R, Turkson J, et al. STATs in oncogenesis[J]. Oncogene, 2000, 19(21) :2474-2488.
  • 3Grandis JR, Drenning SD, Zeng Q, et al. Constitutive activation of STAT3 signaling abrogates apoptosis in squamous cell carcinogenesis in vivo [ J ]. Proc Natl Acad Sci USA, 2000, 97 (8):4227 -4232.
  • 4Schuringa JJ, Wierenga AT, Knfijer W, et al. Constitutive STAT3,Tyr705, and Ser727 phosphorylation in acute myeloid leukemia cells caused by the autocrine secretion of interleukin-6 [ J ].Blood, 2000, 95(12) :3765-3770.
  • 5Badache A, Hynes NE. Interleukin 6 inhibits proliferation and,in cooperation with an epidermal growth factor receptor autocrine loop, increases migration of T47D breast cancer cells [ J ]. CancerRes, 2001,61 ( 1 ) :383-391.
  • 6Buettner R, Mora LB, Jove R. Activated STAT signaling in human tumors provides novel molecular targets for therapeutic intervention[J]. Clin Cancer Res, 2002, 8(4) :945-954.
  • 7Bromberg JF, Horvath CM, Besser D, et al. STAT3 activation is required for cellular transformation by v-src [ J ]. Mol Cell Biol,1998, 18(5) :2553-2558.
  • 8Leong PL, Andrews GA, Johnson DE, et al. Targeted inhibition of STAT3 with a decoy oligonucleotide abrogates head and neck cancer cell growth[J]. Proc Natl Acad Sci USA, 2003,100(7) :4138-4143.
  • 9Huang JS, Guh JY, Hung WC, et al. Role of the Janus kinase(JAK)/signal transducers and activators of transcription (STAT)cascade in advanced glycation end-product-induced cellular mitogenesisNRK-49F cells [J]. Biochem J, 1999, 342( pt 1 ) :231-238.
  • 10Sui G, Soohoo C, Affarel B, et al. A DNA vector-based RNAi technology to suppress gene expression in mammalian cells [ J ].Proc Natl Acad Sci USA, 16, 2002 ,99(8) :5515-5520.

共引文献16

同被引文献176

引证文献16

二级引证文献52

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部