Research Paper Volume 16, Issue 2 pp 1237—1248
Silencing of METTL3 prevents the proliferation, migration, epithelial-mesenchymal transition, and renal fibrosis of high glucose-induced HK2 cells by mediating WISP1 in m6A-dependent manner
Figure 3. Increase of METTL3 expression memorably strengthened EMT progression and fibrosis of HG-induced HK2 cells. Sh-METTL3 or NC were transfected into HG-treated HK2 cells, and OE-METTL3 or vector were transfected into HK2 cells. (A) QRT-PCR and western blot analysis of METTL3 expression in METTL3-silenced HK2 cells after HG induction. (B) QRT-PCR and western blot analysis of METTL3 expression in METTL3-overexpressed HK2 cells. (C) CCK-8 assay demonstrated the change of cell proliferation. (D) The cell migration was credited through the application of wound healing assay. (E) The changes of E-cadherin, Fibronectin and a-SMA expressions were identified using western blot. (F) Western blot assay for the detection of c-MYC, Wnt1 and β-catenin expressions. **P < 0.01, ***P < 0.001.