Fig 1: lncRNA-CASC7 was up-regulated in the peripheral blood monocytes of heart failure patients (*P value <0.05 vs. control group; HF: heart failure; pEF: preserved ejection fraction; rEF: reduced ejection fraction). A, Expression of lncRNA-CCAT1 was not significantly different in the peripheral blood monocytes of HFpEF, HFrEF and control groups. B, Expression of lncRNA-CASC7 was elevated in the peripheral blood monocytes of HFpEF and HFrEF patients. C, Expression of lncRNA-AK017368 was not significantly different in the peripheral blood monocytes of HFpEF, HFrEF and control groups. D, Expression of IL-11 mRNA was not significantly different in the peripheral blood monocytes of HFpEF, HFrEF and control groups
Fig 2: KRT8 is required for the IL-11-mediated metastatic phenotype in ccRCC(A) IL-11 mRNA levels were determined by qRT-PCR, and IL-11, p-STAT3, and STAT3 protein levels were determined by western blotting. (B) IL-11 overexpression restored Caki-1-SH-mediated migration and invasion ability. In contrast, IL-11 knockdown significantly reduced 786-O-KRT8 cell migration and invasion. (C) Representative images of the mice over time after the tail vein injections with each type of renal cancer cell. The statistical analysis is shown in (D). (E) Representative H&E-stained images of the lung metastatic loci in each group in (C). The statistical analysis is shown in (F).
Fig 3: lncRNA-CASC7 was up-regulated in the plasma of heart failure patients (*P value <0.05 vs. control group; HF: heart failure; pEF: preserved ejection fraction; rEF: reduced ejection fraction). A, Expression of lncRNA-CCAT1 was not significantly different in the plasma of HFpEF, HFrEF and control groups. B, Expression of lncRNA-CASC7 was elevated in the plasma of HFpEF and HFrEF patients. C, Expression of lncRNA-AK017368 was not significantly different in the plasma of HFpEF, HFrEF and control groups. D, Expression of IL-11 mRNA was not significantly different in the plasma of HFpEF, HFrEF and control groups
Fig 4: miR-30c inhibited the luciferase activity of the lncRNA-CCAT1 and IL-11 3'UTR plasmid (*P value <0.05 vs. control mimics group; WT: wild type; MUT: mutant). A, Sequence analysis showed a target of miR-30c in lncRNA-CASC7 (Binding site: 235bp-257bp). B, Luciferase activity of WT lncRNA-CASC7 vector was inhibited by miR-30c mimics in H9C2 cells. C, Sequence analysis showed a target of miR-30c in lncRNA- CCAT1 (Binding site: 121bp-145bp). D, Luciferase activity of WT and MT lncRNA-CASC7 vectors was not affected by miR-30c mimics in H9C2 cells. E, Sequence analysis showed a target of miR-30c in lncRNA- AK017368 (Binding site: 235bp-257bp). F, Luciferase activity of WT lncRNA-CASC7 vector was not suppressed by miR-30c mimics in H9C2 cells. G, Sequence analysis showed a target of miR-30c in IL-11 3'UTR (Binding site: 367bp-390bp). H, Luciferase activity of WT IL-11 3'UTR vector was obstructed by miR-30c mimics in H9C2 cells
Fig 5: lncRNA-CASC7 suppressed the expression of miR-30c in H9C2 cells (*P value <0.05 vs. NC group; NC: negative control). A, The successful transfection of plasmids carrying lncRNA-CASC7 led to the overexpression of lncRNA-CASC7 in H9C2 cells. B, Overexpression of lncRNA-CASC7 reduced the expression of miR-30c in H9C2 cells. C, Expression of miR-30c was decreased in H9C2 cells transfected with lncRNA- CCAT1. D, Expression of miR-30c was not affected in H9C2 cells transfected with lncRNA- AK017368. E, Overexpression of lncRNA-CASC7 increased the expression of IL-11 mRNA in H9C2 cells. F, Overexpression of lncRNA-CASC7 increased the expression of IL-11 in H9C2 cells
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