Fig 1: TET2 inhibits proliferation and invasion of NPC cells. a TET1/2/3 mRNA expression levels were examined in several NPC and the immortalized nasopharyngeal cell line NP69 by qRT-PCR. b TET1/2/3 protein expression levels were examined in the indicated cells by western blotting. c Relative mRNA expression level of TET1/3 to TET2. d The knockdown efficiency of siR-TET2 was examined by Western blotting in CNE1 cells. Cell viability of TET2-knockdown CNE1 (e) and SUNE1 (f) cells were examined. Cell invasive ability of TET2-knockdown CNE1 (g) and SUNE1 (h) were examined. Data are represented as mean ± SD (n = 3; *represents P < 0.05)
Fig 2: DEX boosted TET1 and abated OGD/R-mediated DNA methylation in cardiomyocytes.
Fig 3: TET1 overexpression may promote EMT and knockdown of TET1 mitigates hypoxia-induced EMT.(A, B) Western blotting analysis showed the expression of vimentin (Vim) and E-cadherin (E-Cad) in cells transfected with TET1 expression plasmid (TET1) or empty vectors (NC) under normoxia conditions, and cells transfected with TET small interfering RNA (si-TET1) or negative control (si-NC) under hypoxia conditions. (*p < 0.05 versus normoxia+NC; #p < 0.05 versus normoxia+TET1; & p < 0.05 versus hypoxia+si-NC).
Fig 4: miR-21 promoted mFLS cell proliferation and suppressed inflammatory cytokines by repressing TET1. (a) TET1 in each group determined by western blot, *p < 0.05, compared with mimic NC + oe-NC, #p < 0.05, compared with miR-21 mimic + oe-NC. (b) Proliferation determined by EdU labeling, *p < 0.05, compared with mimic NC + oe-NC, #p < 0.05, compared with miR-21 mimic + oe-NC. (c) Proliferation rates of each group determined by CCK-8 assay, *p < 0.05, compared with mimic NC + oe-NC, #p < 0.05, compared with miR-21 mimic + oe-NC. (d) Inflammatory cytokines expression determined by ELISA, *p < 0.05, compared with mimic NC + oe-NC, #p < 0.05, compared with miR-21 mimic + oe-NC.Data are shown as the mean ± standard deviation. Statistical comparisons were performed by Tukey’s test-corrected one-way ANOVA when more than two groups were compared. The experiment was repeated three times.mFLS, mouse fibroblast-like synoviocytes; NC, normal control; oe-NC, overexpressed TET1 or KLF4 control; ELISA, enzyme-linked immuno sorbent assay.
Fig 5: Tet DKO mice show an osteopenia phenotype. a Bone volume/tissue volume (BV/TV) of trabecular bone area in the femurs of control, Tet1−/−, Prx1creTet2fl/fl, and Tet DKO mice were analyzed by micro-CT. b The cortical bone area (Ct.Ar) and cortical thickness (Ct.Th) in the femur of control, Tet1−/−, Prx1creTet2fl/fl, and Tet DKO mice were assessed by micro-CT. c H&E staining showed the trabecular bone volume (yellow-circled area) in the distal femurs of control, Tet1−/−, Prx1creTet2fl/fl, and Tet DKO mice. d Calcein double labeling assay showed the bone formation rate in the metaphyseal trabecular bone of control and Tet DKO mice. The 8–10-week-old Tet1−/−Prx1creTet2fl/fl mice were used as Tet DKO mice in these experiments, and their littermates whose genetic status was Prx1cre were used as controls. *p < 0.05, **p < 0.01, ***p < 0.001 (mean ± SD). Scale bars, 400 μm (a, b), 1 mm (c), and 25 μm (d). Results are from three independent experiments. p values were calculated using one-way ANOVA (a-c) and two-tailed Student's t test (d)
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