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. 2020 Mar 27;28(2):191–201. doi: 10.3727/096504019X15761465603129

Figure 1.

Figure 1

RPSAP52 (ribosomal protein SA pseudogene 52) enhances the binding of miR-15a, miR-15b, and miR-16 to CDKN1A messenger RNAs (mRNAs). (A) RNA immunoprecipitation sequencing (RIPseq) expression profile of anti-AGO2 RIP analysis in HT-29 cells transfected with p-RPSAP52, p-RPSAP52 vector containing mutated binding sites for miR-15a, miR-15b, and miR-16, or empty vector. Normal immunoglobulin Gs (IgGs) and U6 RNA enrichment were used as negative control. Error bars indicate the mean of three independent experiments performed in triplicate. *p < 0.05 compared with HT-29–empty vector-transfected cells immunoprecipitated with an anti-AGO2 antibody. (B) Representation of human CDKN1A 3′-untranslated region (3′-UTR) and the relative position of the predicted microRNA (miRNA) binding sites (http://www.targetscan.org). (C) RIP analysis, assessed by immunoprecipitation of AGO2 in HT-29 cells transfected with p-RPSAP52, p-RPSAP52 vector containing mutated binding sites for miR-15a, miR-15b, and miR-16, or empty vector. IgG and G6PD immunoprecipitation were used as a negative control. *p < 0.05 compared with HT-29–empty vector-transfected cells immunoprecipitated with anti-AGO2 antibody.