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. 2019 Mar 18;8(4):1721–1730. doi: 10.1002/cam4.2040

Figure 2.

Figure 2

CDKN2B‐AS1 can directly interact with miR‐181a‐5p in HeLa cells. (A) Predict binding sites between CDKN2B‐AS1 and miR‐181a‐5p. (B) The expression of miR‐181a‐5p mRNA level was detected in HeLa cells after sh‐CDKN2B‐AS1 transfection with or without miR‐181a inhibitor by qRT‐PCR. U6 was used as the internal control. **P < 0.01, compared with control group. ##P < 0.01, compared with miR‐181a inhibitor group. (C) CDKN2B‐AS1 was constructed on adenovirus packaging vector (Ad‐CDKN2B‐AS1). The expression of miR‐181a‐5p mRNA level was detected in HeLa cells after Ad‐CDKN2B‐AS1 transfection with or without miR‐181a mimic by qRT‐PCR. U6 was used as the internal control. **P < 0.01, compared with control group. ##P < 0.01, compared with miR‐181a mimic group. (D) Luciferase activity was detected by Luciferase reporter assay. HEK 293 T cells were co‐transfected with either 50 nM miR‐181a‐5p mimics or NC oligos and 200 ng of pmirGLO‐CDK‐wt or pmirGLO‐CDK‐mut using Lipofectamine 2000. The relative firefly luciferase activity was measured 24 hours after transfection and was normalized with renilla luciferase activity && P < 0.01 compared with CDK‐wt group. The data shown are the mean ± standard error of three individual experiments. CDK = CDKN2B‐AS1