Supplementary Figures from TET-Mediated Sequestration of miR-26 Drives EZH2 Expression and Gastric Carcinogenesis

Supplementary Figures S1-7. Supplementary Figure S1. Analysis of TET1/2/3 expression and 5-hmC levels in GC specimens and cell lines; Supplementary Figure S2. Effect of TETs on GC cell cycle, apoptosis and invasion; Supplementary Figure S3. Diagram of different recombinant expression vectors containing the TET1/2 5''UTR, the TET1/2/3 CDS, the TET1/2/3 3''UTR and the TET1/2/3 3''UTR with mutation of miR-26 binding sites as well as the TET1/2/3 full-length cDNA; Supplementary Figure S4. The expression levels of TET1, TET2 and TET3 in MKN-28 cells transfected with TET1/2/3 5''UTR, CDS, 3''UTR and full-length cDNA plasmids or empty vector; Supplementary Figure S5. TETs are direct targets of miR-26 in GC cells; Supplementary Figure S6. The regulatory role of TETs in the expression of EZH2; Supplementary Figure S7. TETs co-localize with miR-26 and EZH2 in the cytoplasm of GC cells.