Fig. 2From: METTL3-mediated m6A modification of SIRT1 mRNA inhibits progression of endometriosis by cellular senescence enhancingMETTL3 mediate m6A methylation inhibits the progression of EMs by promoting cellular senescence in vitro and in vivo. A The measurement of the knockdown efficiency of si-METTL3 transfected ESCs in mRNA level by RT-qPCR. B The global m6A levels in si-METTL3 transfected ESCs detected by m6A dot blot assay with anti-m6A antibody. The increasing ability of viability, proliferation, invasion, and migration of ESCs with si-METTL3 transfection was detected by CCK8 C, EdU staining D), wound healing E and Transwell F assay. G The mRNA level of METTL3 in oe-METTL3 transfected ESCs by RT-qPCR. H The mRNA N6-methyladenosine level in oe-METTL3 transfected ESCs by m6A dot blot. I–L CCK8, EdU, wound healing, and Transwell assay showed the decreasing ability of viability, proliferation, invasion, and migration of ESCs with oe-METTL3 transfection in reverse. M Level of cellular senescence in ESCs transfect with si-NC, si-METTL3, oe-vector and oe-METTL3 by SA-β -Gal staining. N The protein level of METTL3 and senescence biomarkers in ESCs transfect with si-NC, si-METTL3, oe-vector, and oe-METTL3 by western blotting, using GAPDH as an internal control. O Mass morphology of AAV-shNC and AAV-shMETTL3 mice. P The xenografts were isolated and measured by caliper in AAV-shNC and AAV-shMETTL3 mice. Xenografts’ weight Q and volume R were measured and analyzed. S Representative staining images for cellular senescence biomarkers (Lamin b1, p53, and p21) in AAV-shNC(up) and AAV-shMETTL3 group(down) by IHC. (Scale bars = 100 μm and 50 μm). All above result were shown in means ± SD, ns, p ≥ 0.05; *p < 0.05; **p < 0.01; ***p < 0.001Back to article page