LncRNA XIST is involved in rheumatoid arthritis fibroblast-like synoviocytes by sponging miR-126-3p via the NF-κB pathway
The role and mechanism of lncRNA XIST (XIST) in the development of rheumatoid arthritis (RA) was explored in this study. RT-qPCRs were performed to detect the expression of XIST and miR-126-3p in synovial tissues and cells. Target gene prediction and luciferase gene reporter assay were used to valid...
Main Authors: | , , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
Taylor & Francis Group
2021-08-01
|
Series: | Autoimmunity |
Subjects: | |
Online Access: | http://dx.doi.org/10.1080/08916934.2021.1937608 |
_version_ | 1827817306427752448 |
---|---|
author | Wei Liu Jing Song Xingyu Feng Haolong Yang Wei Zhong |
author_facet | Wei Liu Jing Song Xingyu Feng Haolong Yang Wei Zhong |
author_sort | Wei Liu |
collection | DOAJ |
description | The role and mechanism of lncRNA XIST (XIST) in the development of rheumatoid arthritis (RA) was explored in this study. RT-qPCRs were performed to detect the expression of XIST and miR-126-3p in synovial tissues and cells. Target gene prediction and luciferase gene reporter assay were used to validate downstream target genes of XIST. MTT assay, EdU staining and Annexin V/PI staining were performed to explore the effects of XIST and miR-126-3p on cell proliferation and apoptosis. Western blotting analysis was used to detect the expression of related proteins. We found that the expression levels of XIST in tissues and cells were significantly higher than that in normal tissues and cells. Down-regulation of XIST could inhibit cell proliferation rate and increase apoptosis rate. Luciferase gene reporter assay showed that miR-126-3p was a downstream target gene of XIST. Overexpression of miR-126-3p significantly inhibited RA-FLS cell proliferation and induced RA-FLS cell apoptosis. In addition, down-regulation of XIST could increase the ratio of caspase-3 and Bax/Bcl-2. In addition, overexpression of miR-126-3p could inhibit the NF-κB signalling pathway by reducing the expression levels of p-p65 and p-IκBα in RA-FLS cells. In conclusion, down-regulation of XIST can inhibit the proliferation of synovial fibroblasts by increasing the expression levels of miR-126-3p/NF-κB, thereby inhibiting the occurrence and development of RA. |
first_indexed | 2024-03-12T00:32:28Z |
format | Article |
id | doaj.art-b97f351cce1045e0a796e289c49a62ca |
institution | Directory Open Access Journal |
issn | 0891-6934 1607-842X |
language | English |
last_indexed | 2024-03-12T00:32:28Z |
publishDate | 2021-08-01 |
publisher | Taylor & Francis Group |
record_format | Article |
series | Autoimmunity |
spelling | doaj.art-b97f351cce1045e0a796e289c49a62ca2023-09-15T10:12:24ZengTaylor & Francis GroupAutoimmunity0891-69341607-842X2021-08-0154632633510.1080/08916934.2021.19376081937608LncRNA XIST is involved in rheumatoid arthritis fibroblast-like synoviocytes by sponging miR-126-3p via the NF-κB pathwayWei Liu0Jing Song1Xingyu Feng2Haolong Yang3Wei Zhong4Department of Rheumatology and Immunology, the First hospital of Qiqihar CityDepartment of Rheumatology and Immunology, the First hospital of Qiqihar CityDepartment of Rheumatology and Immunology, the First hospital of Qiqihar CityDepartment of Orthopedics, the Third Affiliated Hospital of QiqiharDepartment of Rheumatology and Immunology, the First hospital of Qiqihar CityThe role and mechanism of lncRNA XIST (XIST) in the development of rheumatoid arthritis (RA) was explored in this study. RT-qPCRs were performed to detect the expression of XIST and miR-126-3p in synovial tissues and cells. Target gene prediction and luciferase gene reporter assay were used to validate downstream target genes of XIST. MTT assay, EdU staining and Annexin V/PI staining were performed to explore the effects of XIST and miR-126-3p on cell proliferation and apoptosis. Western blotting analysis was used to detect the expression of related proteins. We found that the expression levels of XIST in tissues and cells were significantly higher than that in normal tissues and cells. Down-regulation of XIST could inhibit cell proliferation rate and increase apoptosis rate. Luciferase gene reporter assay showed that miR-126-3p was a downstream target gene of XIST. Overexpression of miR-126-3p significantly inhibited RA-FLS cell proliferation and induced RA-FLS cell apoptosis. In addition, down-regulation of XIST could increase the ratio of caspase-3 and Bax/Bcl-2. In addition, overexpression of miR-126-3p could inhibit the NF-κB signalling pathway by reducing the expression levels of p-p65 and p-IκBα in RA-FLS cells. In conclusion, down-regulation of XIST can inhibit the proliferation of synovial fibroblasts by increasing the expression levels of miR-126-3p/NF-κB, thereby inhibiting the occurrence and development of RA.http://dx.doi.org/10.1080/08916934.2021.1937608rheumatoid arthritislncrna xistmir-126-3pnf-κbapoptosis |
spellingShingle | Wei Liu Jing Song Xingyu Feng Haolong Yang Wei Zhong LncRNA XIST is involved in rheumatoid arthritis fibroblast-like synoviocytes by sponging miR-126-3p via the NF-κB pathway Autoimmunity rheumatoid arthritis lncrna xist mir-126-3p nf-κb apoptosis |
title | LncRNA XIST is involved in rheumatoid arthritis fibroblast-like synoviocytes by sponging miR-126-3p via the NF-κB pathway |
title_full | LncRNA XIST is involved in rheumatoid arthritis fibroblast-like synoviocytes by sponging miR-126-3p via the NF-κB pathway |
title_fullStr | LncRNA XIST is involved in rheumatoid arthritis fibroblast-like synoviocytes by sponging miR-126-3p via the NF-κB pathway |
title_full_unstemmed | LncRNA XIST is involved in rheumatoid arthritis fibroblast-like synoviocytes by sponging miR-126-3p via the NF-κB pathway |
title_short | LncRNA XIST is involved in rheumatoid arthritis fibroblast-like synoviocytes by sponging miR-126-3p via the NF-κB pathway |
title_sort | lncrna xist is involved in rheumatoid arthritis fibroblast like synoviocytes by sponging mir 126 3p via the nf κb pathway |
topic | rheumatoid arthritis lncrna xist mir-126-3p nf-κb apoptosis |
url | http://dx.doi.org/10.1080/08916934.2021.1937608 |
work_keys_str_mv | AT weiliu lncrnaxistisinvolvedinrheumatoidarthritisfibroblastlikesynoviocytesbyspongingmir1263pviathenfkbpathway AT jingsong lncrnaxistisinvolvedinrheumatoidarthritisfibroblastlikesynoviocytesbyspongingmir1263pviathenfkbpathway AT xingyufeng lncrnaxistisinvolvedinrheumatoidarthritisfibroblastlikesynoviocytesbyspongingmir1263pviathenfkbpathway AT haolongyang lncrnaxistisinvolvedinrheumatoidarthritisfibroblastlikesynoviocytesbyspongingmir1263pviathenfkbpathway AT weizhong lncrnaxistisinvolvedinrheumatoidarthritisfibroblastlikesynoviocytesbyspongingmir1263pviathenfkbpathway |