Xiangqun Weng
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Xiangqun Weng has a total of 4 co-authors. Here are the top co-authors by number of shared publications:
- Chen Lin
Department of General Surgery, Fuzong Clinical Medical College, Fujian Medical University, Fuzhou, China
1 shared publication - Lina Sun
Department of Presbyatrics, Fuzhou General Hospital (Dongfang Hospital), Xiamen University, Fuzhou, Fujian 350025, China
1 shared publication - Shenglei Huang
Department of Hepatobiliary Disease, Fuzhou General Hospital (Dongfang Hospital), Xiamen University, Fuzhou, Fujian 350025, China
1 shared publication - Zhixian Wu
Fuzong Clinical Medical College of Fujian Medical University, Fuzhou, China
1 shared publication
Latest Publications
- Open Access
- 15 July 2019
- Published by Wiley in BioMed Research International
- Vol. 2019, 1-9
STC2 Is a Potential Prognostic Biomarker for Pancreatic Cancer and Promotes Migration and Invasion by Inducing Epithelial–Mesenchymal Transition
Aberrant expression of stanniocalcin 2 (STC2) is implicated in cancer development. STC2 acts as a tumor promoter to drive some cancers. However, its contribution to the development of pancreatic cancer remains unclear. This study showed that the expression of STC2 was significantly upregulated in pancreatic cancer tissues. Moreover, its expression was positively correlated with tumor size and lymph node metastasis and negatively correlated with 5-year survival rate of pancreatic cancer patients. Additionally, the expression levels of STC2 were a novel biomarker for predicting overall survival rate after surgery. Furthermore, overexpression of STC2 could promote the proliferation, migration, and invasion of pancreatic cancer cell lines, while knocking down of STC2 led to antiproliferation and antimetastasis activities. Further mechanistic investigations revealed that the expression of STC2 could significantly promote the epithelial–mesenchymal transition (EMT) in pancreatic cancer cells. These data indicated that the overexpression of STC2 in pancreatic cancer contributes to the metastasis through the promotion of EMT, suggesting that STC2 is a potential prognostic biomarker and therapeutic target for pancreatic cancer.
- 15 July 2019
- Published by Wiley in BioMed Research International
- Vol. 2019, 1-9
Open AccessSTC2 Is a Potential Prognostic Biomarker for Pancreatic Cancer and Promotes Migration and Invasion by Inducing Epithelial–Mesenchymal Transition
Aberrant expression of stanniocalcin 2 (STC2) is implicated in cancer development. STC2 acts as a tumor promoter to drive some cancers. However, its contribution to the development of pancreatic cancer remains unclear. This study showed that the expression of STC2 was significantly upregulated in pancreatic cancer tissues. Moreover, its expression was positively correlated with tumor size and lymph node metastasis and negatively correlated with 5-year survival rate of pancreatic cancer patients. Additionally, the expression levels of STC2 were a novel biomarker for predicting overall survival rate after surgery. Furthermore, overexpression of STC2 could promote the proliferation, migration, and invasion of pancreatic cancer cell lines, while knocking down of STC2 led to antiproliferation and antimetastasis activities. Further mechanistic investigations revealed that the expression of STC2 could significantly promote the epithelial–mesenchymal transition (EMT) in pancreatic cancer cells. These data indicated that the overexpression of STC2 in pancreatic cancer contributes to the metastasis through the promotion of EMT, suggesting that STC2 is a potential prognostic biomarker and therapeutic target for pancreatic cancer.