Abstract

Abstract Introduction Emerging evidence revealed the active role played by capillary morphogenesis gene 2 (CMG2) during the disease progression and metastasis of some cancers. It was shown that CMG2 was increased in pancreatic tumours in our previous research. The current study further validated this finding for the expression of CMG2 in pancreatic cancer and also dissected its clinical implication. Method Immunochemical staining of CMG2 was performed on a pancreatic cancer tissue microarray (PA2081, Biomax, n = 104). Clinical relevance of CMG2 was analysed in TCGA pancreatic cancer cohort and gene array data (GSE71729) using ANOVA and Kaplan-Meier analyses. Influence of CMG2 on adhesion to a mesothelial cell monolayer was determined using both Mia-PaCa-2 and PANC-1 cell lines with CMG2 knockdown. Result CMG2 is increased significantly in pancreatic ductal adenomas, P < 0.001 compared with adjacent non-tumour tissues. Higher levels of CMG2 were also revealed in the distant metastases of pancreatic cancer, P < 0.001 compared with both primary tumuors and distant metastasis. Elevated expression CMG2 protein in pancreatic cancers was also observed on the tissue microarray. Patients with higher CMG2 expression tumours had shorter overall survival (median = 15.8 months), P < 0.001 compared with those patients with lower CMG2 expressing tumours (median = 30.4 months). Knockdown of the CMG2 significantly decreased the number of cells which adhere to the mesothelial cells (P < 0.001). Conclusion Elevated CMG2 expression in pancreatic ductal adenocarcinomas is associated with distant metastasis and shorter survival which requires further investigation to shed light on its therapeutic potential. Take-home Message Elevated CMG2 expression in pancreatic ductal adenocarcinomas is associated with distant metastasis and shorter survival.

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