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毛细血管形态发生基因2(CMG2)在胰腺癌疾病进展和腹膜转移中的作用

Implication of Capillary Morphogenesis Gene 2 (CMG2) in the Disease Progression and Peritoneal Metastasis of Pancreatic Cancer.

作者信息

Fang Ziqian, Bunston Carly, Xu Yali, Ruge Fiona, Sui Laijian, Liu Ming, Al-Sarireh Bilal, Griffiths Paul, Murphy Kate, Pugh Matthew R, Hao Chunyi, Jiang Wen G, Ye Lin

机构信息

Cardiff China Medical Research Collaborative, Division of Cancer & Genetics, School of Medicine, Cardiff University, Cardiff CF14 4XN, UK.

Department of Surgery, Morriston Hospital, ABM University Health Board, Swansea SA6 6NL, UK.

出版信息

Cancers (Basel). 2024 Aug 20;16(16):2893. doi: 10.3390/cancers16162893.

Abstract

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.

摘要

毛细血管形态发生基因2(CMG2)介导细胞与基质的相互作用,以促进细胞黏附和迁移。CMG2与乳腺癌、前列腺癌和胃癌的疾病进展有关。本研究旨在确定CMG2在胰腺癌疾病进展和腹膜转移中的作用。从北京大学肿瘤医院收集胰腺肿瘤样本。使用定量PCR测定CMG2表达。在胰腺癌细胞中建立CMG2的敲低和过表达后,检测CMG2对几种细胞功能和对腹膜黏附的影响。通过蛋白质组学分析和药物测试发现CMG2调节的潜在途径。CMG2在胰腺癌组织中上调,并与预后不良相关。CMG2在转移灶和伴有远处转移的原发性肿瘤中增加。CMG2促进细胞-细胞、细胞-基质和细胞-透明质酸黏附,这可能由表皮生长因子受体(EGFR)和黏着斑激酶(FAK)途径激活介导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d87/11352480/c55b01b209b8/cancers-16-02893-g001.jpg

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