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Fig. 9 | Molecular Cancer

Fig. 9

From: Long non-coding RNA UCA1 promotes malignant phenotypes of renal cancer cells by modulating the miR-182-5p/DLL4 axis as a ceRNA

Fig. 9

UCA1 positively regulates DLL4 expression via sponging miR-182-5p. The bioinformation analysis results showed that miR-182-5p and DLL4 have common putative binding sites, showed that the 3’UTR sequence of DLL4 is complementary to the seed sequence of miR-182-5p. Dual-luciferase reporter assay showed DLL4-Wt and miR-182-5p mimics co-transfection significantly inhibited luciferase activity (a). Knockdown of UCA1 decreased DLL4, NICD and Hes1 expression, and increased DLL1, Jag1, Jag2 and Notch1 expression in renal cancer cells (b and c). Overexpressing miR-182-5p decreased the expression of DLL4 and knockdown of miR-182-5p increased DLL4 expression in renal cancer cells (d and e). Overexpressing of DLL4 reversed malignant phenotypes inhibition of renal cancer cells induced by silencing shUCA1. The DLL4 specific vector (pcDNA3.1-DLL4) significantly reversed DLL4 expression inhibition induced by silencing UCA1 in renal cancer cells (f and g). Overexpressing DLL4 significantly reversed cell proliferation inhibition induced by silencing UCA1 (h). Overexpressing DLL4 significantly reversed cell migration inhibition induced by silencing UCA1 (i and j). Overexpressing DLL4 significantly reversed cell apoptosis promotion induced by silencing DLL4 (k and l). Assays were performed in triplicate, and data were shown as mean ± standard deviation (SD) of those biological replicates or samples (*P < 0.05, **P < 0.01)

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