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Pathogenesis of psoriasis via miR‐149‐5p/AKT1axis by long noncoding RNA BLACAT1
BACKGROUND: Psoriasis is a chronic, complicated, and recurrent inflammatory skin disease, whose precise molecular mechanisms need to be further explored. The lncRNA bladder cancer‐associated transcript 1 (BLACAT1) is aberrantly expressed in many cancers and associated with cellular hyperproliferatio...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10170242/ https://www.ncbi.nlm.nih.gov/pubmed/37204030 http://dx.doi.org/10.1111/srt.13339 |
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author | Hua, Xiang Li, JiaZheng Shang, MingWei He, WanMei Gao, PengFei Min, Li Peng, XueBiao |
author_facet | Hua, Xiang Li, JiaZheng Shang, MingWei He, WanMei Gao, PengFei Min, Li Peng, XueBiao |
author_sort | Hua, Xiang |
collection | PubMed |
description | BACKGROUND: Psoriasis is a chronic, complicated, and recurrent inflammatory skin disease, whose precise molecular mechanisms need to be further explored. The lncRNA bladder cancer‐associated transcript 1 (BLACAT1) is aberrantly expressed in many cancers and associated with cellular hyperproliferation and may play a role in the pathogenesis of psoriasis. Thus, this study aimed at identifying the primary mechanism associated with BLACAT1 in psoriasis pathogenesis. MATERIALS AND METHODS: Quantitative reverse transcriptase polymerase chain reaction (qRT‐PCR) was performed to detect the expression of BLACAT1 in psoriasis tissues. Cell proliferation and apoptosis were assessed using cell counting kit‐8 and apoptosis assays, respectively. In vivo experiments and histopathological examinations were performed to investigate the effects of BLACAT1 on psoriasis. Dual‐luciferase Reporter and RNA immunoprecipitation assays were used to evaluate the relationship among BLACAT1 and miR‐149‐5p and AKT1. RESULTS: BLACAT1 was upregulated in psoriasis tissues. Overexpression exacerbated the clinical manifestation of psoriasis and increased the epidermal thickness in imiquimod‐induced mice. BLACAT1 could promote proliferation and inhibit apoptosis of keratinocytes. Further studies demonstrated that BLACAT1 positively regulated AKT1 expression, functioning as a competing endogenous RNA (ceRNA) by sponging miR‐149‐5p. CONCLUSIONS: The combination of lncRNA BLACAT1 and miR‐149‐5p regulates AKT1 expression and promotes psoriasis formation thus may provide a new direction for psoriasis treatment. |
format | Online Article Text |
id | pubmed-10170242 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-101702422023-08-11 Pathogenesis of psoriasis via miR‐149‐5p/AKT1axis by long noncoding RNA BLACAT1 Hua, Xiang Li, JiaZheng Shang, MingWei He, WanMei Gao, PengFei Min, Li Peng, XueBiao Skin Res Technol Original Articles BACKGROUND: Psoriasis is a chronic, complicated, and recurrent inflammatory skin disease, whose precise molecular mechanisms need to be further explored. The lncRNA bladder cancer‐associated transcript 1 (BLACAT1) is aberrantly expressed in many cancers and associated with cellular hyperproliferation and may play a role in the pathogenesis of psoriasis. Thus, this study aimed at identifying the primary mechanism associated with BLACAT1 in psoriasis pathogenesis. MATERIALS AND METHODS: Quantitative reverse transcriptase polymerase chain reaction (qRT‐PCR) was performed to detect the expression of BLACAT1 in psoriasis tissues. Cell proliferation and apoptosis were assessed using cell counting kit‐8 and apoptosis assays, respectively. In vivo experiments and histopathological examinations were performed to investigate the effects of BLACAT1 on psoriasis. Dual‐luciferase Reporter and RNA immunoprecipitation assays were used to evaluate the relationship among BLACAT1 and miR‐149‐5p and AKT1. RESULTS: BLACAT1 was upregulated in psoriasis tissues. Overexpression exacerbated the clinical manifestation of psoriasis and increased the epidermal thickness in imiquimod‐induced mice. BLACAT1 could promote proliferation and inhibit apoptosis of keratinocytes. Further studies demonstrated that BLACAT1 positively regulated AKT1 expression, functioning as a competing endogenous RNA (ceRNA) by sponging miR‐149‐5p. CONCLUSIONS: The combination of lncRNA BLACAT1 and miR‐149‐5p regulates AKT1 expression and promotes psoriasis formation thus may provide a new direction for psoriasis treatment. John Wiley and Sons Inc. 2023-05-10 /pmc/articles/PMC10170242/ /pubmed/37204030 http://dx.doi.org/10.1111/srt.13339 Text en © 2023 The Authors. Skin Research and Technology published by John Wiley & Sons Ltd. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made. |
spellingShingle | Original Articles Hua, Xiang Li, JiaZheng Shang, MingWei He, WanMei Gao, PengFei Min, Li Peng, XueBiao Pathogenesis of psoriasis via miR‐149‐5p/AKT1axis by long noncoding RNA BLACAT1 |
title | Pathogenesis of psoriasis via miR‐149‐5p/AKT1axis by long noncoding RNA BLACAT1 |
title_full | Pathogenesis of psoriasis via miR‐149‐5p/AKT1axis by long noncoding RNA BLACAT1 |
title_fullStr | Pathogenesis of psoriasis via miR‐149‐5p/AKT1axis by long noncoding RNA BLACAT1 |
title_full_unstemmed | Pathogenesis of psoriasis via miR‐149‐5p/AKT1axis by long noncoding RNA BLACAT1 |
title_short | Pathogenesis of psoriasis via miR‐149‐5p/AKT1axis by long noncoding RNA BLACAT1 |
title_sort | pathogenesis of psoriasis via mir‐149‐5p/akt1axis by long noncoding rna blacat1 |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10170242/ https://www.ncbi.nlm.nih.gov/pubmed/37204030 http://dx.doi.org/10.1111/srt.13339 |
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