High expression of WNT7A predicts poor prognosis and promote tumor metastasis in pancreatic ductal adenocarcinoma

Scientific Reports

Ling-ye Tao¹  Jiang-yu Yang¹  Rui-zhe He¹  Min-wei Yang¹  Yong-sheng Jiang¹  Xue-liang Fu¹  Dong-jin Wu²  Kun Zhu³ 

[1] Department of Biliary-Pancreatic Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University;Department of General Surgery, The people’s hospital of Suzhou National New &Hi-Tec Industrial development Zone;Department of Surgery, Shanghai Jiading Central Hospital;

关键词: Pancreatic Ductal Adenocarcinoma (PDAC);    Wnt5a Expression;    Performed Transwell Assays;    PDAC Tissue;    PDAC Patients;   

DOI  :  10.1038/s41598-018-34094-3

来源: DOAJ

【 摘 要 】

Abstract Due to the therapy resistance and frequent metastasis, pancreatic ductal adenocarcinoma(PDAC) remains one of the most malignant carcinoma. WNT7A, an important ligand of Wnt/β-catenin signaling pathways, has a controversial role in tumor development. The role of WNT7A in PDAC remains unclear. In this study, we analyzed the expression pattern of WNT7A at mRNA and protein levels. We found pancreatic cancer tissue demonstrated a significant high WNT7A expression compared with the adjacent non-tumor tissue and the expression of WNT7A positively correlates with poor prognosis and lymph node metastasis. Then, we performed transwell assays and wound healing assays in vitro and found that WNT7A promotes the migration capacity of cancer cells. Furthermore, we explored the underlying mechanism of the WNT7A inducing cell migration. Results showed that up-regulated WNT7A expression inducing higher expression of N-cadherin and lower expression of E-cadherin while the contrast result was shown in the WNT7A knock-down group, which suggested that WNT7A might contribute to an epithelial–mesenchymal transition. Finally, we found that the hypoxia culture condition remarkably increased the WNT7A expression. In conclusion, our work demonstrated that hypoxia induced high expression of WNT7A might promote the cell migration via enhancing the epithelial–mesenchymal transition in PDAC.

【 授权许可】

Unknown