Fig. 5: Intronic miR-181a-5p and miR-181b-5p mediate MIR181A1HG expression in GC. | Oncogene

Fig. 5: Intronic miR-181a-5p and miR-181b-5p mediate MIR181A1HG expression in GC.

From: Long non-coding RNA-MIR181A1HG acts as an oncogene and contributes to invasion and metastasis in gastric cancer

Fig. 5

A MIR181A1HG is the host gene of the MIR181A1 and MIR181B1 that embedded in its second intron and generates mature miR-181a-5p, miR-181a-3p, miR-181b-5p and miR-181b-3p. B–E miR-181a-5p (C) and miR-181b-5p (E) expressions level in GC tissues was significantly higher than that observed in NT. GC, GC tissues; NT, normal tissues. Student’s t-test; **, P < 0.05. F Expression of miR-181a-5p or miR-181b-5p in human GC-derived cells compared with GES-1 cells. ***, P < 0.01, GC cell lines vs. GES-1. G Expression of miR-181a-5p and miR-181b-5p in patients with GC detected by H&E and ISH. Representative images of normal and tumor tissues are shown. Scale bars, 100 μm. H The protein expression of E-cadherin, Vimentin and N-cadherin were measured in AGS and MKN-74 cells after transfection miR-181a-5p or miR-181b-5p mimics or inhibitor or corresponding control. I F-actin cytoskeletal arrangement was examined in AGS cells by fluorescence microscopy. Scale bars, 20 μm. J1/2 The correlation of miR-181a-5p or miR-181b-5p and MIR181A1HG expression levels in GC tissues (J1) and cell lines (J2). K1/2 Expression level of miR-181a-5p or miR-181b-5p following of overexpression (K1) or knockdown (K2) of MIR181A1HG in AGS and MKN-74 cells. L1/2 Expression level of MIR181A1HG following of overexpression (L1) or knockdown (L2) of miR-181a-5p or miR-181b-5p in GC cells. M Actinomycin D (10 μg/mL) was applied to GC cells transfected with m-NC, miR-181a-5p or miR-181b-5p. RNA was extracted at indicated time points to detect the RNA level of MIR181A1HG. *, P > 0.05.

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