| [1] PubMed ID: | 31610202 |
| Disease Name: | capillary hemangioma |
| Sample: | IH tissues |
| Dysfunction Pattern: | Interaction[MEKK3/NF-κB pathway] |
| Validated Method: | Western Blot//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Colony Formation Assay//Transwell Assay |
| Description: | In IH tissues, MALAT1 and MEKK3 were overexpressed while miR-424 was down-regulated. Knockdown of MALAT1 suppressed the expression of MEKK3 and inactivated the IKK/NF-κB pathway by sponging miR-424. Overexpression of MEKK3 in HemEcs reversed the impact of knockdown of MALAT1 and overexpression of miR-424 on the cell proliferation, apoptosis, migration, invasion and tube formation rate. The tumor xenografts experiments demonstrated that silencing MALAT1 significantly inhibited the tumor growth in vivo and Ki-67 in the tumor tissues was also significantly suppressed. |
| Causality: | Yes |
| Causal Description: | Silencing MALAT1 or overexpression of miR-424 significantly inhibited the IH cell proliferation, migration and tube formation, but promoted the cell apoptosis. |
| Clinical-realted Application: | |
| [2] PubMed ID: | 32084582 |
| Disease Name: | capillary hemangioma |
| Sample: | IH tissues |
| Dysfunction Pattern: | regulation[MiR-206 / VEGFA axis] |
| Validated Method: | Western Blot//Wound Healing Assay//CCK8//qRT-PCR//Flow Cytometry//Luciferase Report Assay//Colony Formation Assay//Transwell Assay |
| Description: | The results showed that MALAT1 and VEGFA were high-expressed and miR-206 was low-expressed in IH tissues. Knock-down of MALAT1 inhibits the growth of HemECs through regulating miR-206/VEGFA axis, indicating that MALAT1 is a potential therapeutic mechanism for the treatment of IH. |
| Causality: | Yes |
| Causal Description: | SiMALAT1 negatively affected the cell proliferation, migration, invasion and vasoformation of HemECs and promoted apoptosis of HemECs. |
| Clinical-realted Application: | |
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