| [1] PubMed ID: | 31770435 |
| Disease Name: | Uveal melanoma |
| Sample: | uveal melanoma tissues |
| Dysfunction Pattern: | Regulation[p53 signaling pathway] |
| Validated Method: | qRT-PCR |
| Description: | Highly expressed lncRNA PVT1 and MDM2, yet lowly expressed miR-17-3p, were identified in ocular uveal melanoma tissues versus normal adjacent tissues. Then, dual luciferase reporter gene assay, RNA binding protein immunoprecipitation, and RNA pull-down assays showed that lncRNA PVT1 specifically bound to miR-17-3p, and that MDM2 was a target gene of miR-17-3p. |
| Causality: | Yes |
| Causal Description: | Gain- and loss-of-function studies elucidated that silencing of lncRNA PVT1 or overexpression of miR-17-3p resulted in decreased MDM2 expression and increased transcriptional activity of p53, in addition to inhibiting uveal melanoma cell proliferation, migration, and invasion, yet promoted cell apoptosis in vitro. In addition, lncRNA PVT1 silencing or miR-17-3p overexpression was noted to inhibit tumor growth in vivo. |
| Clinical-realted Application: | |
| [2] PubMed ID: | 31002139 |
| Disease Name: | Uveal melanoma |
| Sample: | UM tissues |
| Dysfunction Pattern: | Interaction[inhibiting EZH2] |
| Validated Method: | Western Blot//CCK8//qRT-PCR//Flow Cytometry//Colony Formation Assay |
| Description: | The expression level of lncRNA PVT1 in UM tissues was remarkably higher than that in the adjacent tissues (p<0.05).The protein expression of EZH2 was suppressed after lncRNA PVT1 knockdown (p<0.05). |
| Causality: | Yes |
| Causal Description: | UM cell proliferation was notably repressed after lncRNA PVT1 knockdown by siRNA. Flow cytometry results indicated that the number of apoptotic UM cells in lncRNA PVT1 knockdown group significantly increased compared with that in the blank control group (p<0.05). |
| Clinical-realted Application: | |
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