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. 2021 Oct 17;12(23):7069–7078. doi: 10.7150/jca.63415

Figure 6.

Figure 6

The PCAT18 could regulate the expression of p16 by interacting with miR-570a-3p, thus inhibiting cell proliferation of GC. A. The RNAup algorithm predicted potential binding of miR-570a-3p to PCAT18 and to p16, with considerable sequence complementary in the indicated regions. B and C. qRT-PCR assays detected the expression of miR-570a-3p after knockdown of PCAT18 and overexpression of PCAT18 in SGC-7901 cells. qRT-PCR assays detected the expression of PCAT18 and p16 after inhibition of miR-570a-3p. D. The 3´UTR of p16 mRNA and full length of PCAT18 were respectively inserted downstream of a luciferase gene. The reporter vector was co-transfected with a renilla luciferase vector (for normalization), which were treated by miR-570a-3p inhibitors or control. The luciferase signals of both reporter genes were significantly increased when cells were treated with miR-570a-3p inhibitors. Mutant 3´UTR of p16 and PCAT18 is not affected by miR-570a-3p. E. The luciferase signal of reporter gene was increased when overexpression of PCAT18. F. RIPs experiments showed that PCAT18 and miR-570a-3p were obviously enriched in Ago2-immunoprecipitation relative to control IgG. G and H. The promotion of p16 by PCAT18 was significantly reversed by miR-570a-3p mimics, by using qPCR assays. MTT assays showed that knockdown of p16 could reverse PCAT18-mediated growth inhibition. *P < 0.05, **P < 0.01.