| [1] PubMed ID: | 31788110 |
| Disease Name: | Glioma |
| Sample: | glioma tissues |
| Dysfunction Pattern: | Interaction[Akt/GSK-3β pathway] |
| Validated Method: | qRT-PCR |
| Description: | In the present study, it was revealed that the expression of RNCR3 was increased in glioma tissues compared with in corresponding adjacent normal tissues. Finally, the results of western blot analyses revealed that knockdown of RNCR3 led to a decrease in the expression levels of phosphorylated Akt and glycogen synthase kinase-3β (GSK-3β), without any clear effect on the expression levels of total Akt and GSK-3β. Collectively, these results suggested that RNCR3 is able to regulate cell proliferation, the cell cycle and cell invasion in glioma, potentially via the Akt/GSK-3β signaling pathway. |
| Causality: | Yes |
| Causal Description: | In addition, the U87 and U251 cell lines were selected to investigate the biological function and potential mechanisms of RNCR3 in glioma, and it was observed that RNCR3 knockdown led to an impairment of the proliferative and invasive abilities of cells; furthermore, G1 phase arrest was induced in glioma cells in vitro. |
| Clinical-realted Application: | Furthermore, increased levels of RNCR3 expression were associated with tumor progression and poor survival rates of patients with glioma. |
| [2] PubMed ID: | 30867254 |
| Disease Name: | Glioma |
| Sample: | glioma tissues,cell lines |
| Dysfunction Pattern: | Expression[lower expressed] |
| Validated Method: | qRT-PCR//Transwell Assay//Western Blot |
| Description: | Moreover, we confirmed levels of LINC00599 expression were decreased in glioma tissues and cell lines compared with matched adjacent normal tissues and normal human astrocytes (NHAs), respectively. |
| Causality: | No |
| Causal Description: | |
| Clinical-realted Application: | |
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