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

Author:

Fang Ziqian1,Bunston Carly1,Xu Yali1,Ruge Fiona1,Sui Laijian1,Liu Ming1,Al-Sarireh Bilal2ORCID,Griffiths Paul3,Murphy Kate3ORCID,Pugh Matthew R.3,Hao Chunyi4ORCID,Jiang Wen G.1ORCID,Ye Lin1ORCID

Affiliation:

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

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

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

4. Key Laboratory of Carcinogenesis and Translational Research, Department of Hepato-Pancreato-Biliary Surgery, Peking University Cancer Hospital & Institute, Beijing 100142, China

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.

Publisher

MDPI AG

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