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Fig. 3 | Molecular Cancer

Fig. 3

From: Mettl14 inhibits bladder TIC self-renewal and bladder tumorigenesis through N6-methyladenosine of Notch1

Fig. 3

Down-expression of Mettl14 in bladder TICs drove decreased m6A modification. a Realtime PCR was performed to detect the expression of m6A-associated genes in 20 peri-tumors, 20 eBC and 20 aBC samples. b 10 bladder cancer samples were used for TIC enrichment and sphere formation, followed by realtime PCR analyses for the expression of indicated genes. c, d Immunohistochemistry for Mettl14 expression in tissue array containing 46 peri-tumors, 20 stage I, 27 stage II and 12 stage III bladder tumors. Typical images were shown in C and quantitative results of m6A modification were shown as scatter diagram (d). e Bladder cancer patients were grouped into Mettl14high and Mettl14low groups, followed by Kaplan–Meier survival analysis. f Mettl14 knockout bladder cancer cells were generated through CRISPR/Cas9 strategy, and knockout efficiency was confirmed by Western blot. g The indicated Mettl14 knockout cells were used for m6A detection. h m6A content in Mettl14 knockout cells was detected by RNA dot blot. i Correlation of m6A modification content and Mettl14 expression. The intensity of m6A and Mettl14 was used for. Pearson correlation coefficient (R) and P-value analyses. j The in vitro RNA N6-adenosine methylation activities of Flag-tagged METTL14 were tested using different RNA probes. *P < 0.05, **P < 0.01, ***P < 0.001, by two-tailed T test

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