Knockdown of AGGF1 inhibits the invasion and migration of gastric cancer via epithelial–mesenchymal transition through Wnt/β-catenin pathway

Han-Hui Yao†,
Ya-Jun Zhao†,
Yi-Fu He,
Da-Bing Huang and
Wei WangEmail author View ORCID ID profile

†Contributed equally

Cancer Cell International201919:41

https://doi.org/10.1186/s12935-019-0765-6

Received: 10 December 2018
Accepted: 21 February 2019
Published: 27 February 2019

Abstract

Background

Angiogenic factor with G-patch and FHA domain 1 (AGGF1), as a newly identified human angiogenic factor, is overexpressed in some types of malignant tumors and closely associated with patient’s prognosis. However, the mechanisms involved in the regulation of AGGF1 in gastric cancer (GC) still remain unclear.

Methods

In this study, AGGF1 level in GC tissues and cell lines was analyzed by western blot and quantitative real-time polymerase chain reaction (qRT-PCR). After knockdown of AGGF expression by RNA interference in GC cell lines MKN-45 and MGC-803, wound healing and transwell assays were conducted to examine the effects of AGGF1 on migration and invasion. Tumor growth was assessed in a mouse xenograft model in vivo. Furthermore, expression levels of epithelial–mesenchymal transition (EMT) biomarkers and involvement of the Wnt/β-catenin pathway were detected by western blot and qRT-PCR.

Results

Compared to those in normal groups, the protein and mRNA of AGGF1 expression levels were significantly higher both in GC tissues and cell lines (all P < 0.05). Knockdown of AGGF1 dramatically inhibited the invasion and migration of MKN-45 and MGC-803 cells (all P < 0.01) in vitro, and suppressed the tumor growth of nude mice xenograft model in vivo. Western blot revealed alterations in EMT biomarkers, suggesting the role of AGGF1 in EMT. Moreover, we found that downregulated expression of AGGF1 attenuated Wnt/β-catenin related protein expression.

Conclusions

Collectively, knockdown of AGGF1 inhibits the invasion and migration of gastric cancer via epithelial–mesenchymal transition through Wnt/β-catenin pathway.