Aquaporin 5 promotes the proliferation and migration of human gastric carcinoma cells
Aquaporin 5 promotes the proliferation and migration of human gastric carcinoma cells
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DOI：
10.1007/s13277-013-0712-4
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发表时间：
2013-06-01
期刊：
影响因子：
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通讯作者：
Lv, Nong-Hua
中科院分区：
文献类型：
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作者：
Huang, Yong-Hong;Zhou, Xiao-Yan;Lv, Nong-Hua
水通道蛋白5(Aquaporin 5，AQP5)促进多种肿瘤的进展和侵袭，但其在胃癌发生中的作用尚不清楚。在此，我们研究了AQP5在人胃癌细胞增殖和迁移中的潜在功能。RT-PCR和Western blotting检测AQP5在人胃癌细胞系中的表达。采用免疫组织化学方法检测AQP5在人胃癌组织及相应正常组织中的表达。用四甲基偶氮唑盐比色法、集落形成实验和伤口愈合实验分析AQP5异位过表达或AQP5抑制剂AZA对AGS细胞增殖和迁移的影响。在人胃癌细胞系MKN45、MKN28、AGS和SGC7901中观察到AQP5基因和蛋白的异质性表达。与相应的正常组织相比，AQP5在胃癌组织中表达上调。AQP5蛋白主要定位于细胞膜。AQP5的过度表达与淋巴结转移密切相关。在体外，AQP5的过表达显著增强，而AZA抑制AQP5则显著抑制AGS细胞的增殖和迁移。我们的数据表明，AQP5可能在人胃癌的发生发展过程中发挥重要作用，并提示AQP5是一种潜在的抗胃癌治疗靶点。
Aquaporin 5 (AQP5) promotes the progression and invasion of several cancers, but its role in the tumorigenesis of human gastric carcinoma (GC) has not been clearly defined. Here, we investigated the potential functions of AQP5 in the proliferation and migration of human GC. RT-PCR and western blotting were used to detect the expression of AQP5 in human GC cell lines. Immunohistochemistry was applied to evaluate the expression of AQP5 in human GC tissues and corresponding normal tissues. Following ectopic overexpression of AQP5 or inhibition of AQP5 by its inhibitor, acetazolamide (AZA), cell proliferation and migration of AGS cells were analyzed by MTT assay, colony formation assay, and wound healing assay. Heterogeneous expression of AQP5 mRNA and protein was observed in human GC cell lines MKN45, MKN28, AGS, and SGC7901. AQP5 was up-regulated in GC tissues in comparison to corresponding normal tissues. AQP5 protein was mainly localized in the cell membrane. Overexpression of AQP5 was correlated with enhanced lymph node metastasis. In vitro, overexpression of AQP5 notably enhanced, while inhibition of AQP5 by AZA significantly attenuated the proliferation and migration of AGS cells. Our data indicate that AQP5 may play an important role in the tumorigenesis and progression of human GC and suggest that AQP5 is a potential therapeutic target against GC.