Skip to main content
Fig. 3 | Stem Cell Research & Therapy

Fig. 3

From: METTL3-mediated m6A modification regulates cell cycle progression of dental pulp stem cells

Fig. 3

METTL3 knockdown induced cell apoptosis and senescence of DPSCs. a shRNA lentiviruses inhibited mRNA and protein expression of METTL3 confirmed by PCR and Western blot. b Representative images of DPSCs after METTL3 knockdown were captured with an inverted microscope. c β-Galactosidase staining was used to detect cell senescence in shCTR and shMETTL3-DPSCs. d Statistical analysis of positive β-galactosidase staining cells in green defined as senescence. e Lentiviral vector of METTL3 overexpression was transduced into DPSCs, and upregulated expression levels of mRNA and protein were confirmed by PCR and Western blot. f CCK8 assay analyzed cell viability of METTL3 knockdown and overexpressed DPSCs. g Flow cytometry of Annexin V/PI staining was employed to analyze the apoptotic rate after METTL3 inhibition and overexpression. h Phosphorylation-p53(Pp53) and p53 in shMETTL3-DPSCs were assayed by Western blot and evaluated by ImageJ. i TUNEL assay analyzed DPSC apoptosis induced by METTL3 knockdown. Quantitative data are represented as mean ± SD (n ≥ 3), Student’s t test. *p < 0.05. **p < 0.01. ***p < 0.001. shMETTL3-1 and METTL3-2 are 2 independent shRNAs used to knockdown METTL3 expression, and shCTR as negative control shRNA. METTL3 is a lentiviral vector constructed for METTL3 overexpression, and CTR as negative control of vector

Back to article page