Gene name: | CIRCLARP4 |
Aging type: | Accelerate |
Aging characteristic: |
Tissue type: | -- |
Cell name: | MHCC97L,HCCLM3 |
Gene ID: | -- |
Category: | ncRNA |
Phenotype: | Hepatocellular carcinoma |
Experimental category: | HL |
PMID: | 30520539 |
Experiment: | Knockdown//Flow cytometry//SA-β-Gal activity assay |
Description: | We performed flow cytometry to analyze the cell cycle distribution.CircLARP4 overexpression caused G1/S cell cycle arrest in MHCC97L, whereas knockdown of circLAPR4 exhibited the opposite effects in HCCLM3 cells.To verify our hypothesis, we performed SA-β-gal staining to determine the cellular senescence. Data showed that the percentage of SA-β-gal-positive cells in circLARP4-overexpressed MHCC97L cells was significantly increased. |
Regulatory pathway: | MIR-761-RUNX3-P53-P21 |
R-AG-Pathway: | -- |
Official symbol(s): | MIR761-RUNX3-TP53-CDKN1A |
Pathway experiment: | Knockdown//Western blot//FISH//RIP//Luciferase reporter assay//Immunohistochemistry |
Pathway description: | Western blotting showed that the expression levels of p53 and p21 were upregulated in circLARP4-overexpressed MHCC97L cells and downregulated in sh-circLARP4 HCCLM3 cells.MiR-761 expression was remarkably decreased in circLARP4-overexpressed MHCC97L cells, while miR-761 expression was elevated in sh-circLARP4 HCCLM3 cells . FISH analysis in HCC cells showed that circLARP4 was co-localized with miR-761 in cytoplasm. Given that high degree of AGO2 occupancy in circLARP4 has been implicated previously,16 we performed RIP for AGO2 in HCC cells and showed higher expression levels of circLARP4 and miR-761 in AGO2 pellet compared to those in the control group . Subsequent luciferase reporter assays demonstrated that miR-761 was a direct target of circLARP4. |
Annotation:
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