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. 2020 Aug 6;11(9):2681–2689. doi: 10.1111/1759-7714.13605

Figure 1.

Figure 1

UCA1 is a direct target candidate of miR‐138/193. (a) The potential miRNAs targeting UCA1 in the region (1395–1433 bp) using bioinformatic analysis. (b) MiR‐138 and miR‐193 mimics were transfected into lung cancer cell lines (A549, H1299, and H1650). The RNA levels of UCA1 (Inline graphic) NC, (Inline graphic) miR‐138, and (Inline graphic) miR‐193 and miRNAs (Inline graphic) NC, (Inline graphic) miR‐138, and (Inline graphic) miR‐193 were tested using real‐time PCR. (c) The antagomirs of miR‐138 or miR‐193 were transfected into lung cancer cells and the corresponding RNA level was examined (Inline graphic) NC, (Inline graphic) anti‐miR‐138, and (Inline graphic) anti‐miR‐193; and (Inline graphic) NC, (Inline graphic) anti‐miR‐138, and (Inline graphic) anti‐miR‐193. (d) Construction of wild‐ and mutant‐type binding sites between UCA1 and miR‐138 or miR‐193 in luciferase reporter vector was conducted. A549, H1299 and H1650 cells were cotransfected with UCA1 and wild‐type or mutant miR‐138 (Inline graphic) NC, (Inline graphic) UCA1‐wt, and (Inline graphic) UCA1‐mut or miR‐193 (Inline graphic) NC, (Inline graphic) UCA1‐wt, and (Inline graphic) UCA1‐mut reporter vector, followed by the measurement of luciferase activities. *P < 0.05.