卡加
生物
Wnt信号通路
MUC1号
癌症研究
连环素
幽门螺杆菌
酪氨酸磷酸化
癌症
癌基因
连环蛋白
信号转导
分子生物学
基因
细胞周期
细胞生物学
生物化学
遗传学
毒力
作者
Udhayakumar Gopal,V. Jayanthi,Niranjali Devaraj,Halagowder Devaraj
摘要
Abstract β‐catenin can function as an oncogene when it is translocated to the nucleus, binds to T‐cell factor (TCF) or lymphoid enhance factor and transactivate its target gene. The mechanism responsible for the activation of Wnt signaling pathway in the Cytotoxin‐associated antigen A ( CagA) Helicobacter pylori ( H. pylori )‐infected gastric carcinoma has not been elucidated. We hypothesize that whether interaction of MUC1 with β‐catenin modulates the Wnt signaling and its target gene cyclinD1 in CagA H. pylori ‐infected gastric carcinoma. The result demonstrate that binding of MUC1 CT with Protein Kinase C δ (PKC δ), tyrosine phosphorylation of MUC1 CT, and CagA are strongly associated with the interaction of MUC1 with β‐catenin in CagA H. pylori ‐infected gastric carcinoma. A statistically significant difference ( χ 2 = 24.49; P < 0.001) was found when the binding of MUC1 CT and β‐catenin was compared to subcellular localization of β‐catenin. We also observed significant statistical correlation ( χ 2 = 14.885; P < 0.001) between the cyclinD1 overexpression and the subcellular localization of β‐catenin. The overexpression of cyclinD1 was significantly higher ( χ 2 = 13.785; P < 0.002) in advanced gastric carcinoma with CagA H. pylori infection. In addition cyclinD1 overexpression was significantly higher ( χ 2 = 37.267; P < 0.001) with the interaction of MUC1 CT with β‐catenin in advanced gastric cancer. These findings indicate that MUC1 CT plays a role in the intracellular signaling through its interaction with β‐catenin and upregulate the Wnt target gene cyclinD1 in CagA H. pylori ‐infected gastric carcinoma. © 2007 Wiley‐Liss, Inc.
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