• No results found

MiRNA-543 promotes osteosarcoma cell proliferation and glycolysis by partially suppressing PRMT9 and stabilizing

N/A
N/A
Protected

Academic year: 2020

Share "MiRNA-543 promotes osteosarcoma cell proliferation and glycolysis by partially suppressing PRMT9 and stabilizing"

Copied!
14
0
0

Loading.... (view fulltext now)

Full text

Figure

Table 1: Relationship between miR-543 and clinical characteristics of osteosarcoma patients
Figure 1: MiR-543 negatively correlated with PRMT9 expression in clinical OS tissues and cell lines
Figure 2: MiR-543 promotes OS cell growth in vitro and in vivo. (A) The effect of miR-543 on OS cell growth was analyzed  using the CCK-8 assay
Figure 3: MiR-543 decreases PRMT9 expression by directly binding to its 3′-UTR. (A) An increasing amount of pre-miR-543  plasmid were transfected into HEK293T cells
+4

References

Related documents

In this study, bioinformat- ics analysis and luciferase assay confirmed that PTEN is a direct target gene of miR-524 and that miR-524 induces proliferation of osteosarcoma

Overexpression of miR-96 promotes cell proliferation by targeting FOXF2 in prostate cancer.. Wu-Ran Wei 1 , Guo-Jun Zeng 2 , Chang Liu 3 , Bing-Wen Zou 4 , Li

In conclusion, this study demonstrated that by directly targeting multiple inhibitors of Wnt/β- catenin pathway, including WIF1 and DKK1, overexpression of miR-543-3p

Here, our study found that miR-25 could pro- mote T-cell acute lymphoblastic leukemia cell proliferation and invasion by directly targeting EphA8. In conclusion, the present

MiR-20a promotes cell proliferation by targeting SRCIN1 in human multiple myeloma.. Zhi-Hui Li 1 , Hui-Ming Zhang 2 , Ling Liu 3 , Yu Wang 1 , Xin-Rong

Inhibition Of miR-520a-3p Promoted Cell Proliferation And Glycolysis In Vitro We subsequently used a miR-520a-3p inhibitor to inhibit the expression of miR-520a-3p in GC

Dove press mir-517a promotes Warburg effect in hcc by directly targeting FBP1.. cell proliferation and colony formation

Furthermore, the miR-17-92 cluster promotes cell proliferation, migration and invasion by competitively binding to QKI2, thereby upregulating β-catenin expression