| [1] PubMed ID: | 33820740 |
| Disease Name: | endometriosis of ovary |
| Sample: | endometrial stromal cells and Ishikawa cells |
| Dysfunction Pattern: | Interaction(miR-424-5p) |
| Validated Method: | Western Blot//Transfection//qRT-PCR//Luciferase Report Assay//Cell Proliferation Assay |
| Description: | The relative expression level of CDKN2B-AS1 was up-regulated in eutopic and ectopic endometria. In endometrial stromal cells and Ishikawa cells, CDKN2B-AS1 overexpression promoted cellular proliferation and invasion, and increased the protein expression of vimentin but decreased the expression of E-cadherin. miR-424-5p was confirmed the target of CDKN2B-AS1 through bioinformatics tools and luciferase reporter assays. In addition, the enhanced effect of cellular phenotype of CDKN2B-AS1 overexpression was significantly attenuated by miR-424-5p overexpression. Furthermore, miR-424-5p was able to directly target AKT3 through luciferase reporter assay. Mechanistically, CDKN2B-AS1 acts as a ceRNA by sponging miR-424-5p and targets AKT3. |
| Causality: | Yes |
| Causal Description: | In endometrial stromal cells and Ishikawa cells, CDKN2B-AS1 overexpression promoted cellular proliferation and invasion, and increased the protein expression of vimentin but decreased the expression of E-cadherin.Furthermore, miR-424-5p was able to directly target AKT3 through luciferase reporter assay. |
| Clinical-realted Application: | |
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