Abstract
We found that SDF-1/CXCR7 axis played an important role in the growth and proliferation of gastric cancer in the previous studies. The objectives of this study were to explore the effects of SDF-1/CXCR7 on the metastatic ability of gastric cancer cells and the possible mechanisms. CXCR7 expression in SGC-7901 gastric cancer cells was stably knocked down via lentiviral vectors. The cell migration and invasion abilities were detected by transwell migration and invasion assays. The expressions of matrix metalloproteinase 2 (MMP-2), MMP-9, vascular endothelial growth factor (VEGF), epithelial-mesenchymal transition (EMT) markers and Akt phosphorylation were detected with real-time PCR and/or western blot. We found that SDF-1 markedly enhanced the migration and invasion abilities of SGC-7901 gastric cancer cells; CXCR7 knockdown inhibited these effects. SDF-1/CXCR7 increased the expressions of MMP-2, MMP-9 and VEGF. SDF-1/CXCR7 also downregulated E-cadherin expression but upregulated N-cadherin, vimentin and Snail expressions, suggesting that SDF-1/CXCR7 could promote the development of EMT in gastric cancer cells. Furthermore, SDF-1/CXCR7 could promote Akt phosphorylation. Our results indicated that SDF-1/CXCR7 enhanced the migration, invasion and EMT of gastric cancer cells and thus CXCR7 supression may be a strategy for inhibiting gastric cancer metastasis.
Highlights
According to Global Cancer Statistics 2018, gastric cancer is the fifth most common malignant tumor worldwide (Bray et al, 2018)
Our current study showed that stromal derived factor-1 (SDF-1) could increase the expressions of matrix metalloproteinase 2 (MMP-2) and MMP-9 in gastric cancer cells through CXCR7, which may be another mechanism by which SDF-1/CXCR7 promotes the migration and invasion ability of gastric cancer cells
Our current study showed that SDF-1 promoted vascular endothelial growth factor (VEGF) expression in gastric cancer cells through CXCR7, suggesting that SDF-1/CXCR7 may promote the angiogenesis of gastric cancer
Summary
According to Global Cancer Statistics 2018, gastric cancer is the fifth most common malignant tumor worldwide (Bray et al, 2018). Many studies have found that SDF-1/CXCR4 axis regulates gastric cancer proliferation, migration, invasion, metastasis and angiogenesis (Xue et al, 2017). CXCR7 expression is upregulated in malignant tumors; CXCR7 affects tumor growth and metastasis and is associated with poor prognosis. Our previous study found that the increased expression of CXCR7 in gastric cancer tissues was correlated with tumor size and lymph node metastasis. Its effects on the metastasis of gastric cancer cells and relevant mechanisms especially the Epithelial-mesenchymal transition (EMT) are not clear. EMT and angiogenesis are important factors in tumor metastasis and targeting them is a potential therapeutic strategy. The current research is mainly to explore the effects of SDF-1/CXCR7 on the migration, invasion, angiogenesis and EMT of gastric cancer cells in vitro
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