食管癌组织中PR-SET7的表达及其与临床特征、增殖细胞核抗原的相关性

摘要
图/表
参考文献
相关文章 (15)

全文: PDF (1634 KB)
输出: BibTeX | EndNote (RIS)

摘要目的探讨赖氨酸甲基转移酶(Lysine methyltransferase, KMT) PR-SET7在食管癌组织中的表达及其与临床特征、增殖细胞核抗原(proliferating cell nuclear antigen,PCNA)之间的相关性。方法选择2010-06至2011-02住院的食管癌患者32例,应用免疫组织化学法检测食管癌组织和癌旁组织中PR-SET7和PCNA的表达,并分析PR-SET7表达量与患者性别、年龄、细胞分化程度、TNM分期和淋巴结转移等临床特征的相关性,以及PR-SET7的表达情况和PCNA指数之间的相关性。结果 PR-SET7及PCNA均以核表达为主,癌组织中PR-SET7及PCNA的表达明显强于癌旁组织,其中PR-SET7高表达率为81.25%,癌旁组织中以低表达为主,高表达率为15.62%(P<0.01);PCNA指数癌组织中为68.12±16.03,癌旁组织38.22±20.56,两者比较差异有统计学意义(P<0.05)。PR-SET7在食管癌中的表达与肿瘤细胞分化程度、TNM分期和淋巴结转移有相关性(P<0.05),与患者的性别、年龄无相关性(P>0.05)。PR-SET7的表达程度和PCNA指数有相关性(r_s=0.551,P=0.001)。结论食管癌组织中PR-SET7异常表达,其表达水平可能与肿瘤的进展、转移及预后密切相关;PR-SET7的表达与PCNA指数有显著相关性,对探讨其作用机制有一定意义。

	服务

	把本文推荐给朋友
	加入我的书架
	加入引用管理器
	E-mail Alert
	RSS
	作者相关文章
	郑建
	马仕昆
	陈建

关键词 ：赖氨酸甲基转移酶, 增殖细胞核抗原, 食管癌, 表达, 预后

Abstract：Objective To investigate the expression of lysine methyltransferase(KMT) PR-SET7 in esophageal carcinoma and its relationship with clinical features and proliferating cell nuclear antigen(PCNA).Methods Immunohistochemistry was used to detect the PR-SET7 and PCNA expressions in esophageal cancer tissues and adjacent normal tissues of 32 cases between June 2010 and February 2011. The correlations between the expression of PR-SET7 and patients’ gender, age, degree of carcinoma tissue differentiation, TNM stages, lymph node metastasis and proliferation of tumor cells were analyzed.Results Immunohistochemistry Results showed that PR-SET7 and PCNA were mainly expressed in nuclear. The expression of PR-SET7 and PCNA in cancerous tissues was significantly stronger than in adjacent tissues. The high expression rate of PR-SET7 was 81.25%, but the expression was mostly low in adjacent tissues, where the high expression rate was 15.62%(P<0.01).PCNA index in cancer tissues was 68.12±16.03, normal tissues was 38.22±20.56,both comparative difference was statistically significint (P<0.05).PR-SET7 protein levels in patients with esophagus carcinoma were correlated with invasive depth and lymph node metastasis (P<0.05) rather than with age or gender (P>0.05).There was a significant correlation between the expression of PR-SET7 and PCNA index (r_s=0.551,P=0.001).Conclusions There is an abnormal expression of PR-SET7 and PCNA during the development and progression of esophageal carcinoma. The expression level may be related to tumor progression, metastasis and prognosis. There is a significant correlation between PR-SET7 and PCNA overexpression in cancer tissues, which is of significance for exploration of the mechanism.

Key words： PR-SET7 PCNA esophageal carcinoma expression prognosis

收稿日期: 2016-10-10

ZTFLH:

R730.2

通讯作者: 马仕昆,E-mail:535435133@qq.com

作者简介: 郑建,博士,主任医师。

引用本文:

郑建,马仕昆,陈建. 食管癌组织中PR-SET7的表达及其与临床特征、增殖细胞核抗原的相关性[J]. 武警医学, 2017, 28(2): 161-164. ZHENG Jian,MA Shikun,and CHEN Jian. Expression of PR-SET7 in esophageal carcinoma and its correlation with clinical features and PCNA index. Med. J. Chin. Peop. Armed Poli. Forc., 2017, 28(2): 161-164.

链接本文:

http://journal08.magtechjournal.com/Jwk_wjyx/CN/ 或 http://journal08.magtechjournal.com/Jwk_wjyx/CN/Y2017/V28/I2/161

[1]	Xiao B, Jing C, Kelly G, et al. Specificity and mechanism of the histone methyltransferase Pr-Set7[J]. Genes Dev, 2005, 19(12): 1444-1454.
[2]	Couture J F, Collazo E, Brunzelle J S, et al. Structural and functional analysis of SET8, a histone H4 Lys-20 methyltransferase [J]. Genes Dev, 2005, 19(12): 1455-1465.
[3]	王静,徐金升. 赖氨酸甲基转移酶SET8结构和功能及其与肿瘤关系的研究进展[J]. 肿瘤防治研究, 2015, 42(4):403-406.
[4]	Takawa M, Cho H S, Hayami S, et al. Histone lysine methyltransferase SETD8 promotes carcinogenesis by deregulating PCNA expression [J]. Cancer Res, 2012, 72(13): 3217-3227.
[5]	李俭杰, 邵云,卫星,等. P53和PCNA的表达与食管癌预后因素的临床观察[J].中国医刊, 2012, 47(5): 58-60.
[6]	McCarty K S Jr, Miller L S, Cox E B, et al. Estrogen receptor analyses. Correlation of biochemical and immunohistochemical methods using monoclonal antireceptor antibodies [J]. Arch Pathol Lab Med, 1985, 109(8): 716-721.
[7]	Oda H, Hubner M R, Beck D B, et al. Regulation of the histone H4 monomethylase PR-Set7 by CRL4(Cdt2)-mediated PCNA-dependent degradation during DNA damage[J]. Mol Cell, 2010, 40(3): 364-376.
[8]	Hsiao K Y,Mizzen C A. Histone H4 deacetylation facilitates 53BP1 DNA damage signaling and double-strand break repair [J]. J Mol Cell Biol, 2013, 5(3): 157-165.
[9]	Oda H, Okamoto I, Murphy N, et al. Monomethylation of histone H4-lysine 20 is involved in chromosome structure and stability and is essential for mouse development [J]. Mol Cell Biol, 2009, 29(8): 2278-2295.
[10]	Brustel J, Tardat M, Kirsh O, et al. Coupling mitosis to DNA replication : the emerging role of the histone H4-lysine 20 methyltransferase PR-Set7 [J]. Trends Cell Biol, 2011, 21(8): 452-460.
[11]	Huen M S, Sy S M, Van Deursen J M, et al. Direct interaction between SET8 and proliferating cell nuclear antigen couples H4-K20 methylation with DNA replication [J]. J Biol Chem, 2008, 283(17):11073-11077.
[12]	West L E, Roy S, Lachmi-Weiner K, et al. The MBT repeats of L3MBTL1 link SET8-mediated p53 methylation at lysine 382 to target gene repression [J]. J Biol Chem, 2010, 285(48): 37725-37732.
[13]	Beck D B, Oda H, Shen S S, et al. PR-Set7 and H4K20me1:at the crossroads of genome integrity, cell cycle, chromosome condensation, and transcription[J]. Genes Dev, 2012, 26(4): 325-337.
[14]	Kaniskan H U, Jin J. Chemical probes of histone lysine methyltransferases[J]. ACS Chem Biol, 2015, 10(1): 40-50.
[15]	Copeland R A, Moyer M P, Richon V M, Targeting genetic alterations in protein methyltransferases for personalized cancer therapeutics [J]. Oncogene, 2013, 32(8): 939-946.
[16]	Klose R J, Zhang Y. Regulation of histone methylation by demethylimination and demethy lation [J]. Nat Rev Mol Cell Biol, 2007, 8(4): 307-318.
[17]	Okumura H, Uchikado Y, Setoyama T, et al. Biomarkers for predicting the response of esophageal squamous cell carcinoma to neoadjuvant chemoradiatgion therapy [J]. Surg Today, 2014, 44(3): 421-428.