天津医药

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PIK3CA在胃癌病变中表达的研究

马菲菲1,张庆瑜2,王涛3,徐蓉1   

  1. 1. 天津医学高等专科学校
    2. 天津医科大学总医院消化内科
    3. 天津医大总医院消化科
  • 收稿日期:2013-04-02 修回日期:2013-08-04 出版日期:2013-11-15 发布日期:2013-11-15
  • 通讯作者: 张庆瑜

The Expression of PIK3CA in Gastric Adenocarcinoma

MA Feifei1,ZHANG Qing yu2,WANG Tao2,XU Rong3   

  1. 1. Academic Department of Tianjin Medical Colleg
    2. Department of Gastroenterology, General Hospital of Tianjin Medical University
    3. Academic Department of Tianjin Medical College
  • Received:2013-04-02 Revised:2013-08-04 Published:2013-11-15 Online:2013-11-15
  • Contact: ZHANG Qing yu

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摘要：

【摘要】目的  研究磷脂酰肌醇3－激酶催化亚基α（PIK3CA）表达与胃癌发病及不同病理级别胃肿瘤的关系，探讨其在胃癌发病中的作用机制。 方法  应用组织芯片技术结合免疫组化方法检测PIK3CA、丝氨酸/苏氨酸蛋白激酶（pAkt）、细胞增殖相关核抗原（ki-67）在胃腺癌、癌旁组织、正常胃黏膜中的表达情况,分析其与肿瘤发生的关系；进一步分析PIK3CA、pAkt、ki-67在不同胃癌病理级别组织中的表达情况,及其与肿瘤病理分级、分化的关系。 结果  PIK3CA、pAkt、ki-67在胃癌组织中的表达显著增高（P<0.05），且在低分化胃腺癌中的表达最高（P<0.05），PIK3CA、pAkt和ki-67在不同病理级别胃癌及癌旁组织和正常胃黏膜组织中的表达两两之间呈正相关（P<0.05）。 结论  PIK3CA可能作为磷脂酰肌醇3－激酶/蛋白激酶B(PI3K/Akt)信号通路的始动因子，促使Akt磷酸化，进而激活PI3K/Akt信号传导途径，促进胃癌增殖、侵袭与转移。

关键词: 胃肿瘤, 腺癌, 1-磷脂酰肌醇3-激酶, 蛋白质丝氨酸苏氨酸激酶, ki-67抗原, 免疫组织化学, 组织芯片

Abstract:

[Abstract]  Objective   To investigate the relationship between phosphatidylinositol3- kinase catalytic subunitα
(PIK3CA) expression and the incidence and different pathological grade of gastric cancer, and the mechanism thereof.   Methods   The expressions of PIK3CA, serine/threonine protein kinase (pAkt) and cell proliferation associated nuclear antigen(ki-67) in gastric carcinoma and adjacent tissues and normal gastric mucosa were detected by immunohistochemical method. The relationship between expressions of PIK3CA, pAkt and ki-67and tumorigenesis was analyzed. The expressions of PIK3CA, pAkt and ki-67in different pathological conditions of gastric tissues were analyzed. The relationship between tumor pathologic classification and differentiation were analyzed too. Results  There were significantly higher expressions of PIK3CA, pAkt and ki-67in gastric cancer (P<0.05), which were the highest in the poorly differentiated gastric adenocarcinoma (P<0.05). There were a positive correlation between expressions of PIK3CA, pAkt and ki-67and different pathological levels of gastric carcinoma and adjacent tissues and normal gastric tissues (P<0.05).  Conclusion   PIK3CA may be the initiating factor of PI3K/Akt signaling pathway, which induced phosphorylation of Akt and activation PI3K/Akt signaling pathway, promoting the proliferation, invasion and metastasis of gastric adenocarcinoma.

Key words: stomach neoplasms, adenocarcinoma, 1-phosphatidylinositol 3-kinase, protein-serine-threonine kinases, ki-67antigen, immunohistochemistry, tissue microarrays