CAJ | 학술논문

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。
목적：연구린지선기순3-격매최화아기α（PIK3CA）표체여위암발병급불동병리급별위종류적관계，탐토기재위암발병중적작용궤제。방법응용조직심편기술결합면역조화방법검측PIK3CA、사안산/소안산단백격매（pAkt）、세포증식상관핵항원（ki-67）재위선암、암방조직、정상위점막중적표체정황，분석기여종류발생적관계；진일보분석PIK3CA、pAkt、ki-67재불동위암병리급별조직중적표체정황，급기여종류병리분급、분화적관계。결과 PIK3CA、pAkt、ki-67재위암조직중적표체현저증고（P<0.05），차재저분화위선암중적표체최고（P<0.05）， PIK3CA、pAkt화ki-67재불동병리급별위암급암방조직화정상위점막조직중적표체량량지간정정상관（P<0.05）。결론 PIK3CA가능작위린지선기순3-격매/단백격매B(PI3K/Akt)신호통로적시동인자，촉사Akt린산화，진이격활PI3K/Akt신호전도도경，촉진위암증식、침습여전이。
Objective To investigate the relationship between phosphatidylinositol 3-kinase catalytic subunit α(PIK3CA) expression and the incidence and different pathological grade of gastric cancer, and the mechanism thereof. Meth-ods 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-67 and tumorigenesis was analyzed. The expressions of PIK3CA, pAkt and ki-67 in different pathological conditions of gastric tissues were analyzed. The relationship between tu-mor pathologic classification and differentiation were analyzed too. Results There were significantly higher expressions of PIK3CA, pAkt and ki-67 in gastric cancer (P<0.05), which were the highest in the poorly differentiated gastric adenocarci-noma (P<0.05). There were a positive correlation between expressions of PIK3CA, pAkt and ki-67 and different pathologi-cal 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.