Retraction Note to: CXCL12/CXCR4 Axis Upregulates Twist to Induce EMT in Human Glioblastoma

In recent decades, the chemokine receptor CXCR4and its ligand CXCL12 have been extensively reported to be associated with tumorigenesis. In addition, Twistsignaling induces the epithelial-mesenchymal transition(EMT) process in glioblastomadevelopment. In the present study, in vitro assays were used to investigate the role of CXCR4and Twistin human glioblastoma. We explored the impact of CXCR4and Twiston human glioblastomausing in vitro protein and gene assays. We found the administration of CXCL12 upregulated the expression of p-ERK, p-AKT, Twist, N-cadherin, and MMP9in U87cells, whereas the increase of E-cadherin protein was affected. Subsequently, Twistactivity and EMT signaling were directly influenced by PD98059 and LY294002. Most importantly, the genetic silencing of Twistinhibited CXCL12-induced EMT occurrence, including proliferation, migration, and tumor formation of U87cells. In conclusion, CXCL12/ CXCR4pathway activates ERK and PI3K/AKT signaling to upregulate Twistpathway, leading to the progression of EMT in human glioblastoma. Our study creates a new stage for molecule-targeted therapy of human glioblastoma.