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. 2018 Jun 15;11:3461–3473. doi: 10.2147/OTT.S164131

Figure 5.

Figure 5

MALAT1 acted as a ceRNA of miR-1 to sequester miR-1 away from KRAS in PC cells.

Notes: (A) Predicted binding sites of miR-1 and KRAS 3′-UTR, and mutant sites of KRAS 3′-UTR in WT-KRAS reporter. (B) Effects of miR-1 overexpression and deficiency on luciferase activity of WT-KRAS or MUT-KRAS reporter were determined using a dual-luciferase assay in DU145 cells at 48 h posttransfection. (C) DU145 cells were transfected with miR-NC, miR-1, anti-miR-NC, or anti-miR-1, followed by the measurement of KRAS protein expression at 48 h upon transfection. (D) DU145 cells were cotransfected with WT-KRAS reporter and miR-1 mimic, miR-1+pcDNA3.1, or miR-1+pcDNA-MALAT1, followed by the detection of luciferase activity at 48 h after transfection. (E) DU145 cells were transfected with pcDNA3.1, pcDNA-MALAT1, MALAT1+miR-NC, and MALAT1+miR-1, followed by the examination of KRAS protein expression at 48 h after transfection. *P<0.05.

Abbreviations: ceRNA, competing endogenous RNA; MALAT1, metastasis-associated lung adenocarcinoma transcript 1; PC, prostate cancer; UTR, untranslated region.