Fig 2: miR‐206 inhibits proliferation and invasion by targeting DNMT3A in LSCC cells. (A) DNMT3A expression was suppressed in LSCC cells transfected siRNA against DNMT3A, and this could be partly rescued by the cotransfection of miR‐206 inhibitors. LSCC cells transfected with siRNA against DNMT3A reduced the ability of proliferation (B) and invasion (C), and the effect could be rescued by the cotransfection of miR‐206 inhibitors as our data suggested that miR‐206 binds to DNMT3A to negatively regulate cell proliferation and invasion

Fig 3: Ablation of DNMT3A in skeletal muscle does not affect the whole-body response to high-fat feeding.(A) 18-week-old male WT and mD3AKO mice were fed a HFD for a period of 12 weeks after which body composition and glucose tolerance was determined. Indirect calorimetry was performed at 14 weeks of HFD. (B) Body weight, (C) fat mass, (D) oral glucose tolerance test curves and (E) the area under the curve of the oGTT curves. The mean of the chow values is depicted by the dotted line, n = 9–12. (F) Respiratory exchange ratio and (G) energy expenditure, n = 6. (H) Dnmt3a expression in the soleus, EDL and quadriceps muscles of WT chow and HFD-fed mice compared to the housekeeping gene 18S, fold-change compared to WT, n = 9–10. Analysed by individual t-tests. * P < 0.05. Data show the mean (bar) with individual data points or mean +SD.

Fig 4: Effect of HMD on the expression of DNMT1 and DNMT3a proteins in cortex in mice. (a) Showed representative photomicrographs of DNMT1 and DNMT3a proteins expression of each group in cortex. (b) The protein expression levels of DNMT1 in cortex. (c) The protein expression levels of DNMT3a in cortex. Note: value was expressed as mean ± SEM (n = 4). ∗p < 0.05 vs. control group.

Fig 5: MTA1 modulation of DNMT3a target genes.(A) Western blot showing secreted IGFBP-3 in the conditioned medium from MCF-7 and MCF-7/T7-MTA1 cells; ponceau staining was used to show the equal loading of protein. (B) Western blot showing the IGFBP3 levels from MCF-7 and MCF-7/T7-MTA1 cells. β-actin is shown as the loading control. (C) qPCR analysis of IGFBP-3 in MTA1 overexpressed MCF-7 cells as compared with the vector control. Results were represented in fold change normalized to mRNA levels of 18 S rRNA. (D) qPCR analysis of IGFBP-3 in MTA1+/+ and MEF MTA1−/− MEFs. (E) qPCR showing the levels of DNMT3a and HMMR mRNAs in MCF-7 and in MCF-7 cells overexpressing DNMT3a-YFP or pcDNA3.1 as a vector control. (F) qPCR analysis of HMMR mRNAs in wild-type and MEF MTA1−/− MEFs. Results are presented as fold change after normalizing with β-actin. (G) qPCR analysis of MTA1 and HMMR mRNAs in MCF-7 and in MTA1 overexpressing MCF-7 cells. Results are presented as fold change after normalizing with β-actin.