Fig 1: GATA6-AS1 regulates OC via a miR-19a-5p/TET2 axis. ES-2 cells were transfected with pcDNA-NC, pcDNA-GATA6-AS1, pcDNA-GATA6-AS1 + miR-19a-5p mimics or pcDNA-GATA6-AS1 + sh-TET2. SKOV-3 cells were transfected with sh-NC, sh-GATA6-AS1, sh-GATA6-AS1 + miR-19a-5p inhibitors or pcDNA-GATA6-AS1 + pcDNA-TET2. Subsequently, the mRNA and protein expression levels of TET2 in OC cells were detected using (A) RT-qPCR and (B) western blotting, respectively. (C) Proliferation of OC cells was assessed using a Cell Counting Kit-8 assay. (D) Transwell assays were used to evaluate OC cell migratory and invasive abilities. All experiments were performed in triplicate. *P<0.05, **P<0.01 and ***P<0.001. GATA6-AS1, GATA6 antisense RNA 1; OC, ovarian cancer; miR, microRNA; TET2, ten eleven translocation 2; RT-qPCR, reverse transcription-quantitative PCR; NC, negative control; sh, short hairpin.
Fig 2: TET2 is the target gene of miR-19a-5p in OC cells. (A) TargetScan analysis predicted the presence of a binding site between the 3'UTR of TET2 and miR-19a-5p. (B) Dual luciferase reporter gene assay was used to confirm the binding relationship between miR-19a-5p and TET2. (C) Expression of TET2 in OC and adjacent normal tissues was detected using RT-qPCR. (D) Expression of TET2 in cell lines was detected using RT-qPCR. (E) Expression of TET2 in cell lines was detected using western blotting. (F) miR-19a-5p mimics and inhibitors were transfected into ES-2 and SKOV-3 cells, respectively, and the expression levels of TET2 was detected using RT-qPCR. (G) miR-19a-5p mimics and inhibitors were transfected into ES-2 and SKOV-3 cells, respectively, and the expression levels of TET2 was detected using western blotting. (H) Relationship between expression of miR-19a-5p and TET2 was examined using Pearson's correlation analysis. n=40. All experiments were performed in triplicate. **P<0.01 and ***P<0.001. miR, microRNA; OC, ovarian cancer; TET2, ten eleven translocation 2; UTR, untranslated region; RT-qPCR, reverse transcription-quantitative PCR; MUT, mutant; WT, wild-type; NC, negative control; in, inhibitor.
Fig 3: TET2 is highly expressed in keloid tissue. (A and B) The mRNA level of TET1, TET2 and TET3 in normal skin and keloid tissue were detected by Q-PCR; (C) Dot blot was used to detect the level of 5hmC in the normal and keloid tissue DNA. (D) Relative band intensity of picture C detected grey scanning. **p < 0.01, ***p<0.001.
Fig 4: TET2 regulates the 5hmC in the TGFß promoter region. (A) The TGFß mRNA level in HDFs after vector transfection 48h which was detected Q-PCR. (B) After enrichment of 5hmC by co-immunoprecipitation, the target DNA residue was detected by Q-PCR. (C) The protein level of TGFß in the DNMT3A over-expressed strain that was transfected with shTET2. (D) Relative band intensity of picture C detected grey scanning ***p<0.001.
Fig 5: Low TET2 expression inhibits HKFs proliferation. (A) TET2 mRNA level detected by Q-PCR after knockdown level. (B) TET2 protein level detected by Western blot after knockdown. (C) Relative band intensity of picture B detected grey scanning. (D) Proliferation rate of HKFs in the control group and shTET2 transfected group which were detected by CCK-8. (E) Pictures of EDU incorporation assay and DAPI staining of the control group and shTET2 transfected HKFs. (F) Statistics of picture (E) Fraction of EDU+ cells in DAPI+ cells of the control group and shTET2 group. The more of the values are, the more proliferation rate it stands for. **p < 0.01, ***p<0.001.
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