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miR-183-3p suppresses proliferation and migration of keratinocyte in psoriasis by inhibiting GAB1
BACKGROUND: MicroRNAs (miRNAs) target genes involved in the hyperproliferation of keratinocytes or immune dysfunction of psoriasis. This study prospectively determined the involvement of miR-183-3p in the pathogenesis of psoriasis. METHODS: Differentially expressed miR-183-3p between psoriatic lesio...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7353791/ https://www.ncbi.nlm.nih.gov/pubmed/32650835 http://dx.doi.org/10.1186/s41065-020-00138-w |
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author | Liu, Ting Zhang, Xiaoyan Wang, Yujuan |
author_facet | Liu, Ting Zhang, Xiaoyan Wang, Yujuan |
author_sort | Liu, Ting |
collection | PubMed |
description | BACKGROUND: MicroRNAs (miRNAs) target genes involved in the hyperproliferation of keratinocytes or immune dysfunction of psoriasis. This study prospectively determined the involvement of miR-183-3p in the pathogenesis of psoriasis. METHODS: Differentially expressed miR-183-3p between psoriatic lesional and non-lesional skin were determined by quantitative RT-PCR and in situ hybridization (ISH). CCK8 and wound healing assays were performed to assess cell viability and migration of human keratinocyte cell line (HaCaT). The target of miR-183-3p was validated by luciferase activity assay. RESULTS: Lower miR-183-3p expression was observed in psoriatic lesional skin compared to psoriatic non-lesional skin. MiR-183-3p over-expression inhibited the viability and migration of HaCaT cells, while inhibition of miR-183-3p promoted the viability and migration of HaCaT cells. Moreover, miR-183-3p could bind to the 3′ UTR of GAB1 (growth factor receptor binding 2-associated binding protein 1) and decrease the mRNA and protein expression of GAB1 in HaCaT cells. In addition, higher GAB1 expression was observed in psoriatic lesional skin than psoriatic non-lesional skin. CONCLUSION: MiR-183-3p exhibited inhibition property in the proliferation and migration of HaCaT cells via down-regulation of GAB1, suggesting the potential therapeutic strategy for psoriasis. |
format | Online Article Text |
id | pubmed-7353791 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-73537912020-07-15 miR-183-3p suppresses proliferation and migration of keratinocyte in psoriasis by inhibiting GAB1 Liu, Ting Zhang, Xiaoyan Wang, Yujuan Hereditas Research BACKGROUND: MicroRNAs (miRNAs) target genes involved in the hyperproliferation of keratinocytes or immune dysfunction of psoriasis. This study prospectively determined the involvement of miR-183-3p in the pathogenesis of psoriasis. METHODS: Differentially expressed miR-183-3p between psoriatic lesional and non-lesional skin were determined by quantitative RT-PCR and in situ hybridization (ISH). CCK8 and wound healing assays were performed to assess cell viability and migration of human keratinocyte cell line (HaCaT). The target of miR-183-3p was validated by luciferase activity assay. RESULTS: Lower miR-183-3p expression was observed in psoriatic lesional skin compared to psoriatic non-lesional skin. MiR-183-3p over-expression inhibited the viability and migration of HaCaT cells, while inhibition of miR-183-3p promoted the viability and migration of HaCaT cells. Moreover, miR-183-3p could bind to the 3′ UTR of GAB1 (growth factor receptor binding 2-associated binding protein 1) and decrease the mRNA and protein expression of GAB1 in HaCaT cells. In addition, higher GAB1 expression was observed in psoriatic lesional skin than psoriatic non-lesional skin. CONCLUSION: MiR-183-3p exhibited inhibition property in the proliferation and migration of HaCaT cells via down-regulation of GAB1, suggesting the potential therapeutic strategy for psoriasis. BioMed Central 2020-07-10 /pmc/articles/PMC7353791/ /pubmed/32650835 http://dx.doi.org/10.1186/s41065-020-00138-w Text en © The Author(s) 2020 Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Liu, Ting Zhang, Xiaoyan Wang, Yujuan miR-183-3p suppresses proliferation and migration of keratinocyte in psoriasis by inhibiting GAB1 |
title | miR-183-3p suppresses proliferation and migration of keratinocyte in psoriasis by inhibiting GAB1 |
title_full | miR-183-3p suppresses proliferation and migration of keratinocyte in psoriasis by inhibiting GAB1 |
title_fullStr | miR-183-3p suppresses proliferation and migration of keratinocyte in psoriasis by inhibiting GAB1 |
title_full_unstemmed | miR-183-3p suppresses proliferation and migration of keratinocyte in psoriasis by inhibiting GAB1 |
title_short | miR-183-3p suppresses proliferation and migration of keratinocyte in psoriasis by inhibiting GAB1 |
title_sort | mir-183-3p suppresses proliferation and migration of keratinocyte in psoriasis by inhibiting gab1 |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7353791/ https://www.ncbi.nlm.nih.gov/pubmed/32650835 http://dx.doi.org/10.1186/s41065-020-00138-w |
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