| [1] PubMed ID: | 33389493 |
| Disease Name: | Keloid |
| Sample: | keloid tissues and fibroblasts |
| Dysfunction Pattern: | Interaction(miR-769-5p/EIF3A pathway) |
| Validated Method: | Western Blot//Transfection//Migration Assay//Flow Cytometry//qRT-PCR//MTT//Luciferase Report Assay//Invasion Assay//Transwell Assay |
| Description: | Our study found that lncRNA H19 expression was increased in keloid tissues and fibroblasts. Further experiments showed that microRNA (miR)-769-5p could be sponged by H19, and its knockdown reversed the suppression effect of H19 knockdown on keloid formation. Eukaryotic initiation factor 3A (EIF3A) was found to be a target of miR-769-5p, and its overexpression inverted the inhibition effect of miR-769-5p overexpression on keloid formation. |
| Causality: | Yes |
| Causal Description: | Besides, H19 knockdown hindered the proliferation, migration, invasion, extracellular matrix (ECM) deposition, and enhanced the apoptosis of keloid fibroblasts. |
| Clinical-realted Application: | |
| [2] PubMed ID: | 34974806 |
| Disease Name: | Keloid |
| Sample: | keloid tissue and fibroblasts |
| Dysfunction Pattern: | Interaction(miR-196b-5p/SMAD5) |
| Validated Method: | qRT-PCR |
| Description: | H19 and SMAD5 expression was upregulated in keloid tissue and fibroblasts, whereas miR-196b-5p expression was downregulated. miR-196b-5p was identified as a H19 sponge, and SMAD5 was identified as a miR-196b-5p target. |
| Causality: | Yes |
| Causal Description: | Knockdown of H19, overexpression of miR-196b-5p, or knockdown of SMAD5 inhibited the viability and proliferation of keloid fibroblasts and promoted apoptosis. Overexpression of H19 or SMAD5 and knockdown of miR-196b-5p promoted viability and proliferation and inhibited apoptosis. |
| Clinical-realted Application: | |
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