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Fig. 5 | Journal of Experimental & Clinical Cancer Research

Fig. 5

From: ADAR1 promotes the epithelial-to-mesenchymal transition and stem-like cell phenotype of oral cancer by facilitating oncogenic microRNA maturation

Fig. 5

ADAR1 could bind to Dicer and promote the maturation of oncogenic miRNAs. a Representative image of Co-IP. Cell lysates were incubated with normal rabbit IgG, anti-ADAR1, anti-Dicer, anti-Drosha, anti-Argonaute1, anti-Argonaute2, and anti-TRBP antibodies. b Representative image of immunofluorescence indicated that ADAR1 and Dicer were co-located in Cal27 cells. Scale bar: 20 μm. c ADAR1 overexpression upregulated oncogenic miRNAs. d ADAR1 overexpression decreased the precursor levels of six oncogenic miRNAs. e ADAR1 overexpression decreased the primary levels of six oncogenic miRNAs. f ADAR1-p110 knockdown reduced oncogenic miRNAs and tumor suppressor miRNAs expression. g Dicer knockdown inhibited oncogenic miRNAs and tumor suppressor miRNAs expression. The data were expressed as the mean ± SEM (n ≥ 3). *p < 0.05; **p < 0.01; ***p < 0.00; #p > 0.05

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