KCNQ1OT1 promotes the proliferation and migration of psoriatic keratinocytes by regulating miR-183-3p/GAB1
| Autor: | Chuan Yang, Jia He, Xi Duan, Ting Liu |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Pulmonary and Respiratory Medicine
Keratinocytes Gene knockdown business.industry Tumor Necrosis Factor-alpha Immunology General Medicine Cell biology HaCaT Growth factor receptor binding MicroRNAs medicine.anatomical_structure Cell culture Potassium Channels Voltage-Gated microRNA medicine Immunology and Allergy Humans MTT assay RNA Long Noncoding Viability assay Keratinocyte business Adaptor Proteins Signal Transducing Cell Proliferation |
| Zdroj: | Allergologia et immunopathologia. 49(5) |
| ISSN: | 1578-1267 |
| Popis: | Background: Differentially expressed long non-coding RNAs (lncRNA) have been reported to be involved in the proliferation and migration of keratinocyte. Potassium voltage-gated channel subfamily Q member 1 overlapping transcript 1 (KCNQ1OT1) was implicated in the pathogenesis of various diseases, including cancer, sepsis, diabetic cardiomyopathy, and atherosclerosis. In this study, the influence of KCNQ1OT1 on the proliferation and migration of psoriatic keratinocytes was explained. Methods: Cultured human keratinocyte cell line (HaCaT) was incubated with tumor necrosis factor-α (TNF-α). Cell viability and migration were assessed by MTT assay and wound healing, respectively. Target miRNA of KCNQ1OT1 was identified by luciferase activity and RNA immunoprecipitation (RIP) assays. Results: KCNQ1OT1 was up-regulated in TNF-α-treated HaCaT cell line, and knockdown of KCNQ1OT1 reduced viability and suppressed the migration of TNF-α-treated HaCaT cell line. KCNQ1OT1 was bound to microRNA-183-3p (miR-183-3p) and negatively regulated its expression. Over-expression of growth factor receptor binding 2-associated binding protein 1 (GAB1) counteracted with the suppressive effects of KCNQ1OT1-induced silence on the viability and migration of TNF-α-treated HaCaT cells. Conclusion: KCNQ1OT1 silence suppressed the proliferation and migration of TNF-α-treated HaCaT cells through regulation of miR-183-3p/GAB1. |
| Databáze: | OpenAIRE |
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