Conclusion
Therefore, this study may provide a theoretical foundation for further clinical therapy of gastric cancer.
Methods
qPCR and Western blot were performed to determine the expression of ANTXR1 after KLF7 inhibition. CCK-8, colony formation, apoptosis analysis, cell cycle analysis and transwell assay were performed to determine KLF7 functions in cellular proliferation, migration, apoptosis and cell cycle. Tumour xenograft experiments were performed to examine cell growth in vivo.
Purpose
Elucidating the mechanism of gastric cancer progression is of great importance for the discovery of new therapy targets against gastric cancer. In this study, we investigated the function of Kruppel-like factor 7 (KLF7) in gastric cancer.
Results
The results showed that KLF7 was upregulated in gastric cancer. The proliferation and migration of gastric cancer cells were suppressed by depletion of KLF7. In vivo tumour progression was also attenuated following the downregulation of KLF7. Meanwhile, overexpression of KLF7 promoted the proliferation and migration of gastric cancer cells. The results of the mechanistic analysis showed that KLF7 promoted gastric carcinogenesis via upregulation of ANTXR cell adhesion molecule 1 (ANTXR1).