| [1] PubMed ID: | 34895065 |
| Disease Name: | Carcinoma, Hepatocellular |
| Sample: | HCC cell line |
| Dysfunction Pattern: | Interaction(miR-5195-3p/FOXO1) |
| Validated Method: | CCK8//qRT-PCR//Transwell Assay |
| Description: | Compared with normal tissues, MEG3 expression was significantly downregulated in HCC tissues. Double luciferase reporter and RNA pull-down assays confirmed the binding between MEG3 and miR-5195-3p as well as between miR-5195-3p and FOXO1. RT-qPCR and Western blotting results showed that MEG3 inhibited the expression of miR-5195-3p and promoted that of FOXO1. Additionally, MEG3 overexpression inhibited HCC tumorigenesis and progression in xenograft tumor models while depletion of MEG3 exerted the opposite way. |
| Causality: | Yes |
| Causal Description: | MEG3 overexpression inhibited the viability and migration of HCC cells. |
| Clinical-realted Application: | |
| [2] PubMed ID: | 33747202 |
| Disease Name: | Carcinoma, Hepatocellular |
| Sample: | HCC cell |
| Dysfunction Pattern: | Interaction(miR-9-5p/MDK axis ) |
| Validated Method: | CCK8//qRT-PCR//Western Blot |
| Description: | The present study demonstrated that MEG3 suppressed HCC cell viability and migration, and induced cell apoptosis. In addition, it was also found that MEG3 targets the miR-9-5p/MDK axis and modulates the PDK/AKT pathway in HCC. |
| Causality: | Yes |
| Causal Description: | In conclusion, the findings of the present study demonstrated that lncRNA MEG3 affects HCC cell viability, apoptosis and migration through its targeting of miR-9-5p/MDK and regulation of the PDK/AKT pathway. |
| Clinical-realted Application: | |
| [3] PubMed ID: | 31531526 |
| Disease Name: | Carcinoma, Hepatocellular |
| Sample: | HCC tissues and cell lines |
| Dysfunction Pattern: | Interaction[sponging miR-9-5p to upregulate SOX11] |
| Validated Method: | qRT-PCR//Luciferase Report Assay//RNA Pull-Down//Western Blot |
| Description: | The results showed that MEG3 and SOX11 were poorly expressed but miR-9-5p was highly expressed in HCC. The results showed that MEG3 and SOX11 were poorly expressed but miR-9-5p was highly expressed in HCC. The expression levels of these molecules suggested a negative correlation between MEG3 and miR-9-5p and a positive correlation with SOX11, confirmed by Pearson's correlation analysis and biology experiments. Furthermore, MEG3 could combine with miR-9-5p, and SOX11 was a direct target of miR-9-5p. Moreover, MEG3 over-expression promoted cell apoptosis and growth inhibition in HCC cells through sponging miR-9-5p to up-regulate SOX11. Therefore, the interactions among MEG3, miR-9-5p, and SOX11 might offer a novel insight for understanding HCC pathogeny and provide potential diagnostic markers and therapeutic targets for HCC. |
| Causality: | Yes |
| Causal Description: | Moreover, MEG3 over-expression promoted cell apoptosis and growth inhibition in HCC cells through sponging miR-9-5p to up-regulate SOX11. |
| Clinical-realted Application: | |
| [4] PubMed ID: | 31089680 |
| Disease Name: | Carcinoma, Hepatocellular |
| Sample: | hepatocellular carcinoma tissues |
| Dysfunction Pattern: | Interaction[upregulating TGF-β1] |
| Validated Method: | CCK8//qRT-PCR//Transwell Assay |
| Description: | The results showed that expression level of MEG3 was significantly lower in tumor tissues than in adjacent healthy tissues.We also found that MEG3 small interfering Ribonucleic Acid (siRNA) silencing promoted the proliferation, migration, and invasion of hepatocellular carcinoma cells by CCK-8 assay, transwell migration, and invasion assay, respectively, while TGF-β inhibitor treatment reduced those enhancing effects. MEG3 siRNA silencing also increased the expression level of TGF-β1. These results indicated that downregulation of MEG3 can promote proliferation, migration, and invasion of human hepatocellular carcinoma cells by upregulating TGF-β1 expression. |
| Causality: | Yes |
| Causal Description: | We also found that MEG3 small interfering Ribonucleic Acid (siRNA) silencing promoted the proliferation, migration, and invasion of hepatocellular carcinoma cells by CCK-8 assay, transwell migration, and invasion assay, respectively, while TGF-β inhibitor treatment reduced those enhancing effects. |
| Clinical-realted Application: | |
| [5] PubMed ID: | 31396320 |
| Disease Name: | Carcinoma, Hepatocellular |
| Sample: | HCC tissues |
| Dysfunction Pattern: | Regulation[PTEN/AKT/MMP-2/MMP-9 signaling axis] |
| Validated Method: | qRT-PCR//Luciferase Report Assay//Western Blot |
| Description: | Compared to carcinoma-adjacent regions, MEG3 expression was downregulated in cancer regions of HCC samples; by contrast, miRNA-10a-5p was overexpressed in cancer regions compared to tumor-adjacent areas.Furthermore, miRNA-10a-5p bound the 3-untranslated region of PTEN mRNA and downregulated PTEN protein expression. Taken together, these data suggest that MEG3 regulates the PTEN/AKT/MMP-2/MMP-9 signaling axis and contributes to HCC development by targeting miRNA-10a-5p. |
| Causality: | Yes |
| Causal Description: | Furthermore, overexpression of MEG3 (a) decreased proliferation, migration, and invasion of HepG2 cells; (b) enhanced apoptosis and the proportion of HepG2 cells in G1 of the cell cycle |
| Clinical-realted Application: | |
| [6] PubMed ID: | 35049008 |
| Disease Name: | Carcinoma, Hepatocellular |
| Sample: | HCC patients |
| Dysfunction Pattern: | Mutation(rs7158663 ) |
| Validated Method: | qRT-PCR |
| Description: | The AA, GA+AA, and A alleles were associated with increased risk for HCC (adjusted odds ratio (OR) 11.84%, 95% CI 4.07-34.45, p < 0.0001; adjusted OR 3.18, 95% CI 1.79-5.67, p < 0.0001; and adjusted OR 2.87, 95% CI 1.91-4.34, p < 0.0001, respectively). MEG3 serum expression level was downregulated in HCC patients. The rs7158663 G > A polymorphism and downregulated MEG3 were significantly associated with larger tumor size and advanced disease stage. |
| Causality: | No |
| Causal Description: | |
| Clinical-realted Application: | The mutant genotype and allele were linked to an increased risk in male patients and patients ≥ 50 years old. |
| [7] PubMed ID: | 36553522 |
| Disease Name: | Carcinoma, Hepatocellular |
| Sample: | cell lines and tumors |
| Dysfunction Pattern: | Interaction(miR664a-3p/ADH4 Axis) |
| Validated Method: | qRT-PCR |
| Description: | Maternally Expressed Gene 3 (MEG3) is an imprinted lncRNA that is reported to be downregulated in HCC (in both cell lines and tumors). Alcohol Dehydrogenase 4 (ADH4) is a well-known prognostic protein biomarker for predicting the survival outcomes of patients with hepatocellular carcinoma whose expression is regulated by miR-664a-3p, which is upregulated in HCC.In summary, our interaction analyses results predict the significance of the MEG3/miR-664a-3p/ADH4 axis, where MEG3 downregulation results in miR-664a-3p overexpression and the subsequential underexpression of ADH4 in HCC, as a novel axis of interest that demands further validation. |
| Causality: | No |
| Causal Description: | |
| Clinical-realted Application: | |
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