Connexin32 inhibits gastric carcinogenesis through cell cycle arrest and altered expression of p21Cip1 and p27Kip1.
Connexin32 inhibits gastric carcinogenesis through cell cycle arrest and altered expression of p21Cip1 and p27Kip1.
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DOI：
10.5483/bmbrep.2013.46.1.078
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发表时间：
2013-01
期刊：
影响因子：
3.8
通讯作者：
Kim DY
中科院分区：
文献类型：
--
作者：
Jee H;Lee SH;Park JW;Lee BR;Nam KT;Kim DY
缝隙连接及其结构蛋白连接蛋白（Cxs）与肿瘤发生有关。为探讨Cx 32在胃癌发生发展中的作用，采用组织微阵列技术对胃癌组织和正常组织中Cx 32和增殖标志物Ki 67进行免疫组化分析。另外，通过溴脱氧尿苷法、流式细胞术、实时荧光定量PCR和Western印迹法检测Cx 32过表达于人胃癌细胞系AGS后细胞增殖、细胞周期以及p21 Cip 1和p27 Kip 1表达水平的变化。免疫组化结果显示，Cx 32和Ki 67的表达模式与它们的位置呈强负相关。在体外，Cx 32在AGS细胞中的过表达显著抑制细胞增殖。G1期阻滞，细胞周期调控蛋白p21 Cip 1和p27 Kip 1在mRNA和蛋白水平上表达上调。综上所述，Cx 32通过细胞周期阻滞和细胞周期调控蛋白抑制胃癌细胞增殖，在胃癌的发生发展中发挥一定的作用。[BMB报告2013; 46（1）：25-30]
Gap junctions and their structural proteins, connexins (Cxs), have been implicated in carcinogenesis. To explore the involvement of Cx32 in gastric carcinogenesis, immunochemical analysis of Cx32 and proliferation marker Ki67 using tissue-microarrayed human gastric cancer and normal tissues was performed. In addition, after Cx32 overexpression in the human gastric cancer cell line AGS, cell proliferation, cell cycle analyses, and p21Cip1 and p27Kip1 expression levels were examined by bromodeoxyuridine assay, flow cytometry, real-time RT-PCR, and western blotting. Immunohistochemical study noted a strong inverse correlation between Cx32 and Ki67 expression pattern as well as their location. In vitro, overexpression of Cx32 in AGS cells inhibited cell proliferation significantly. G1 arrest, up-regulation of cell cycle-regulatory proteins p21Cip1 and p27Kip1 was also found at both mRNA and protein levels. Taken together, Cx32 plays some roles in gastric cancer development by inhibiting gastric cancer cell proliferation through cell cycle arrest and cell cycle regulatory proteins. [BMB Reports 2013; 46(1): 25-30]
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