Fig. 6: TINCR recruits DNMT1 to miR-503-5p promoter to regulate miR-503-5p gene methylation. | Cell Death & Disease

Fig. 6: TINCR recruits DNMT1 to miR-503-5p promoter to regulate miR-503-5p gene methylation.

From: LncRNA TINCR favors tumorigenesis via STAT3–TINCR–EGFR-feedback loop by recruiting DNMT1 and acting as a competing endogenous RNA in human breast cancer

Fig. 6: TINCR recruits DNMT1 to miR-503-5p promoter to regulate miR-503-5p gene methylation.

a TINCR knockdown increases Pri-MiR-503-5p and Pre-MiR-503-5p expression in UACC 812 cells. b Schematic representation of predicted CpG island in miR-503-5p locus. CpG island located in the promoter region of miR-503-5p locus around the transcriptional start site (TSS, −310 to +92 bases; “−”: upstream of TSS; “+”: downstream of TSS). c Pri-MiR-503-5p and Pre-MiR-503-5p expression is upregulated in UACC 812 and MDA-MB-231 cells treated with decitabine (1 μM) for 10 h. d MiR-503-5p expression is upregulated in UACC-812 and MDA-MB-231 cells treated with decitabine (1 μM) for 10 h. e miR-503-5p expression is upregulated in UACC 812 and MDA-MB-231 cells following DNMT1 knockdown. f ChIP assay results indicating that DNMT1 is enriched at miR-503-5p locus CpG islands in UACC 812 and MDA-MB-231 cells. g RIP-assay results showing higher enrichment of TINCR in DNMT1 group than IgG group in UACC 812 and MDA-MB-231 cells. IgG: negative control. h ChIP assay results indicating diminished enrichment of DNMT1 at the promoter of miR-503-5p locus after TINCR knockdown. Data are presented as means from three independent experiments ± S.D. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, ###P < 0.001.

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