含FXYD域离子运输调控因子3对人胰腺癌细胞增殖和迁移的影响

Effect of FXYD domain-containing ion transport regulator 3 on proliferation and migration of human pancreatic cancer cells

  • 摘要:
    目的 探讨含FXYD域离子运输调控因子3(FXYD3)对人胰腺癌细胞增殖和迁移的影响。
    方法 使用免疫组化法、组织病理学和实时荧光定量聚合酶链反应(qRT-PCR)检测21例正常胰腺组织、18例慢性胰腺炎组织和50例胰腺癌组织中FXYD3的表达。分析不同病理特征的胰腺癌中FXYD3的表达水平差异。采用CCK-8法和单克隆实验法检测FXYD3过表达对胰腺癌细胞增殖的影响; 采用Transwell法检测FXYD3过表达对胰腺癌细胞侵袭的影响。
    结果 FXYD3阳性细胞在正常胰腺组织、慢性胰腺炎组织和胰腺癌组织样本中的比率分别为0、22.2%和26.0%, FXYD3阳性细胞在慢性胰腺炎组织和胰腺癌组织中的比率较正常胰腺组织中升高, 差异有统计学意义(P=0.007、0.037)。FXYD3阳性表达与分期、病理分级、淋巴结转移情况以及肿瘤部位无相关性(P>0.05)。CCK-8法结果显示, FXYD3转染的细胞从第3天开始显示出更强的增殖能力, 差异有统计学意义(P < 0.01)。平板克隆实验显示, FXYD3过表达的T3M4细胞克隆数目更多, 差异有统计学意义(P < 0.01)。Transwell法结果显示, FXYD3过表达的T3M4细胞迁移数目较对照组上升, 差异有统计学意义(P < 0.05)。
    结论 胰腺癌组织中FXYD3显著上调, 这主要是由于癌细胞自身表达水平的增高, 表明FXYD3促进胰腺癌细胞的增殖。

     

    Abstract:
    Objective  To explore the effect of FXYD domain-containing ion transport regulator 3 (FXYD3) on the proliferation and migration of human pancreatic cancer cells.
    Methods  Immunohistochemistry, histopathology and real-time quantitative fluorescent polymerase chain reaction (qRT-PCR) were used to detect the expression of FXYD3 in 21 cases with normal pancreas tissues, 18 cases with chronic pancreatitis tissues and 50 cases with pancreatic cancer tissues. The differences of FXYD3 expression level in pancreatic cancer with different pathological characteristics were analyzed. Effect of FXYD3 overexpression on the proliferation of pancreatic cancer cells were detected by CCK-8 assay and monoclonal assay; the Transwell method was used to detect the effect of FXYD3 overexpression on the invasion of pancreatic cancer cells.
    Results  The ratios of FXYD3 positive cells in samples of normal pancreatic tissues, chronic pancreatitis tissues and pancreatic cancer tissues were 0, 22.2% and 26.0% respectively, and the ratio of FXYD3 positive cells in chronic pancreatitis tissues and pancreatic cancer tissues was significantly higher than that in normal pancreatic tissues (P=0.007, 0.037). There were no correlations of FXYD3 positive expression with staging, pathological grading, lymph node metastasis and tumor sites (P>0.05). The result of CCK-8 method showed that the cells transfected with FXYD3 had significant stronger proliferative ability from the third day (P < 0.01). Colony formation assay showed that the clonal number of T3M4 cells overexpressed with FXYD3 was significantly greater (P < 0.01). The result of Transwell method showed that the migratory number of T3M4 cells overexpressed with FXYD3 was significantly greater than that of the control group (P < 0.05).
    Conclusion  FXYD3 is significantly up-regulated in pancreatic cancer tissues, which is mainly due to the increase of self-expressed level of cancer cells, indicating that FXYD3 can promote the proliferation of pancreatic cancer cells.

     

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