Capillary morphogenesis gene 2 (CMG2) mediates cell–matrix interactions to facilitate cell adhesion and migration. CMG2 has been implicated in the disease progression of breast cancer, prostate cancer and gastric cancer. The present study aims to determine the role of CMG2 in the disease progression and peritoneal metastasis of pancreatic cancer. Pancreatic tumour samples were collected from Peking University Cancer Hospital. CMG2 expression was determined using quantitative PCR. After the creation of knockdown and overexpression of CMG2 in pancreatic cancer cells, the effect of CMG2 on several cell functions and adhesion to the peritoneum was examined. Potential pathways regulated by CMG2 were found via proteomics analysis and drug tests. CMG2 was upregulated in pancreatic cancer tissues and associated with a poor prognosis. CMG2 was increased in metastatic lesions and those primary tumours with distant metastases. CMG2 promotes cell–cell, cell–matrix and cell–hyaluronic acid adhesion, which may be mediated by epidermal growth factor receptor (EGFR) and focal adhesion kinase (FAK) pathway activation.
毛细血管形态发生基因2(CMG2)介导细胞-基质相互作用,促进细胞黏附与迁移。已有研究表明CMG2参与乳腺癌、前列腺癌及胃癌的疾病进展。本研究旨在探讨CMG2在胰腺癌疾病进展及腹膜转移中的作用。胰腺肿瘤样本取自北京大学肿瘤医院,通过定量PCR检测CMG2表达水平。在胰腺癌细胞中构建CMG2敲低与过表达模型后,检测CMG2对多种细胞功能及腹膜黏附能力的影响,并通过蛋白质组学分析与药物实验探索CMG2调控的潜在通路。结果显示:CMG2在胰腺癌组织中表达上调且与不良预后相关;其在转移病灶及伴有远处转移的原发肿瘤中表达显著升高;CMG2通过激活表皮生长因子受体(EGFR)与黏着斑激酶(FAK)通路,促进细胞-细胞、细胞-基质及细胞-透明质酸的黏附作用。