[1] PubMed ID: | 35987744 |
Disease Name: | Keloid |
Sample: | tissues and fibroblasts of keloid |
Dysfunction Pattern: | Interaction(miR-182-5p on ZNF217) |
Validated Method: | In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Wound Healing Assay//qPCR//CCK8//Flow Cytometry//RIP//Luciferase Report Assay//Bioinformatics Analysis |
Description: | HOXA11-AS was highly expressed in tissues and fibroblasts of keloid. Deficiency of HOXA11-AS blocked the proliferation and migration of keloid fibroblasts and induced fibroblast apoptosis. HOXA11-AS directly combined to miR-182-5p whose downregulation reversed the effects of HOXA11-AS knockdown. ZNF217 was a target of miR-182-5p, and HOXA11-AS indirectly promoted ZNF217 expression by binding to miR-182-5p. MiR-182-5p enrichment also blocked keloid fibroblast proliferation, survival and migration, while further ZNF217 overexpression abolished these effects. HOXA11-AS knockdown also hindered the growth of keloid in mouse models. |
Causality: | Yes |
Causal Description: | Deficiency of HOXA11-AS blocked the proliferation and migration of keloid fibroblasts and induced fibroblast apoptosis. HOXA11-AS directly combined to miR-182-5p whose downregulation reversed the effects of HOXA11-AS knockdown. ZNF217 was a target of miR-182-5p, and HOXA11-AS indirectly promoted ZNF217 expression by binding to miR-182-5p. MiR-182-5p enrichment also blocked keloid fibroblast proliferation, survival and migration, while further ZNF217 overexpression abolished these effects. HOXA11-AS knockdown also hindered the growth of keloid in mouse models. |
Clinical-realted Application: | |
[2] PubMed ID: | 33261854 |
Disease Name: | Keloid |
Sample: | keloid tissues and keloid fibroblasts |
Dysfunction Pattern: | Interaction(miR-205-5p-FOXM1 Pathway) |
Validated Method: | Western Blot//Bioinformatics Analysis//Transfection//Migration Assay//qRT-PCR//RIP//Luciferase Report Assay//Cell Apoptosis Assay//Cell Proliferation Assay//Invasion Assay |
Description: | HOXA11-AS and FOXM1 were significantly upregulated in keloid tissues and keloid fibroblasts, while miR-205-5p was downregulated. MiR-205-5p was targeted by HOXA11-AS, and its inhibition overturned the effects of HOXA11-AS knockdown. Moreover, FOXM1 was a target of miR-205-5p, and HOXA11-AS regulated the expression of FOXM1 by adsorbing miR-205-5p. |
Causality: | Yes |
Causal Description: | HOXA11-AS knockdown or miR-205-5p enrichment inhibited proliferation, migration, invasion, ECM accumulation, and glycolysis but accelerated apoptosis of keloid fibroblasts. |
Clinical-realted Application: | |
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