Fig. 6: miR-181a-5p and miR-181b-5p influence MIR181A1HG transcription and regulate the invasion of GC by directly targeting SOCS3 mRNA. | Oncogene

Fig. 6: miR-181a-5p and miR-181b-5p influence MIR181A1HG transcription and regulate the invasion of GC by directly targeting SOCS3 mRNA.

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

Fig. 6

A The Venn diagram indicates the numbers of genes that overlapped in seven public available bioinformatics algorithms (miRanda, miRmap, MS-miroT, PITA, StarBase, TargetScan, microT-CDS). Thirty-six genes were potential targets of miR-181a-5p and miR-181b-5p. B Expression of ABI1, SOCS3, SENP2, KLF15 and DUSP5 genes was analyzed in AGS cells by qRT-PCR. *, P > 0.05, ***, P < 0.01, and ****, P < 0.001. C Western blotting of SOCS3 levels treated with NC, miR-181a-5p or miR-181b-5p mimic or inhibitor in GC cells. D The putative miR-181a-5p and miR-181b-5p- binding site in the SOCS3 3’-UTR. The replaced site is underlined. E1/2 Relative luciferase activity of the reporter constructs harboring WT or MT 3’-UTR of SOCS3 upon co-transfection with m-NC, miR-181a-5p or miR-181b-5p mimic (E1), or i-NC, miR-181a-5p or miR-181b-5p inhibitor (E2) in GC cells. WT, wildtype; MT, mutated. *, P > 0.05, and ****, P < 0.001. F Ago2-RIP was conducted to detect endogenous RNA binding to Ago2; IgG was employed as the control. The levels of miR-181a-5p, miR-181b-5p and SOCS3 were detected by qRT-PCR, and shown as fold-enrichment in Ago2 compared to lgG. ****, P < 0.001. G The RIP assays were performed using Ago2 or IgG to estimate the enrichment of SOCS3 mRNA in AGS cells transfected with miR-181a-5p or miR-181b-5p mimics or m-NC. ***, P < 0.01, and ****, P < 0.001. (H) Invasion and migration assays were conducted using transfected AGS cells. (I) Wound healing assays were used to detect GC cell motility in AGS cells.

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