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. 2019 May 2;39(5):BSR20181465. doi: 10.1042/BSR20181465

Figure 4. The up-regulation of UCA1 impairs the inhibitory effect of miR-204 on CXCR4 expression.

Figure 4

(A) The left panel showed the expression level of UCA1 in the PC-3 treated with 1 μg, 10 μg of UCA1 plasmids or control plasmids. The right panel showed mRNA level of CXCR4 in control and PC-3 cells treated with miR-204 alone or together with UCA1 plasmids (1 or 10 μg). (B) The protein level of β-catenin, pERK1/2, pAKT in control and PC-3 cells treated with miR-204 alone or together with 1 μg of UCA1 plasmids. Mann–Whitney U test was used to compare relative ratio between control and treated groups. (C) The expression correlation of UCA, CXCR4, and miR-204 in PCa tissues (n=40). Spearman’s rank correlation (r) was used for the correlation analysis. (D) A proposed mechanistic model as to how UCA1 functions as a miR-204 sponge and regulates CXCR4 via inhibiting miR-204 activity. The persistent up-regulation of UCA1 sequestered miR-204 and thereby lead to the accumulation of CXCR4 signaling to drive colorectal tumor growth.