Long non-coding RNA KCNQ1OT1 promotes cell viability and migration as well as inhibiting degradation of CHON-001 cells by regulating miR-126-5p/TRPS1 axis
Abstract Background Osteoarthritis (OA) is defined as a degenerative disease. Pivotal roles of long non-coding RNA (lncRNAs) in OA are widely elucidated. Herein, we intend to explore the function and molecular mechanism of lncRNA KCNQ1OT1 in CHON-001 cells. Methods Relative expression of KCNQ1OT1, m...
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| Format: | Article |
| Language: | English |
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BMC
2021-06-01
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| Series: | Advances in Rheumatology |
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| Online Access: | https://doi.org/10.1186/s42358-021-00187-3 |
| _version_ | 1819099930690584576 |
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| author | Binfeng Wang Xiangwei Liu |
| author_facet | Binfeng Wang Xiangwei Liu |
| author_sort | Binfeng Wang |
| collection | DOAJ |
| description | Abstract Background Osteoarthritis (OA) is defined as a degenerative disease. Pivotal roles of long non-coding RNA (lncRNAs) in OA are widely elucidated. Herein, we intend to explore the function and molecular mechanism of lncRNA KCNQ1OT1 in CHON-001 cells. Methods Relative expression of KCNQ1OT1, miR-126-5p and TRPS1 was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability was examined by MTT assay. The migratory ability of chondrocytes was assessed by transwell assay. Western blot was used to determine relative protein expression of collagen II, MMP13 and TRPS1. Dual-luciferase reporter (DLR) assay was applied to test the target of lncRNA KCNQ1OT1 or miR-126-5p. Results Relative expression of KCNQ1OT1 and TRPS1 was reduced, whereas miR-126-5p was augmented in cartilage tissues of post-traumatic OA patients compared to those of subjects without post-traumatic OA. Increased KCNQ1OT1 or decreased miR-126-5p enhanced cell viability and migration, and repressed extracellular matrix (ECM) degradation in CHON-001 cells. MiR-126-5p was the downstream target of KCNQ1OT1, and it could directly target TRPS1. There was an inverse correlation between KCNQ1OT1 and miR-126-5p or between miR-126-5p and TRPS1. Meantime, there was a positive correlation between KCNQ1OT1 and TRPS1. The promoting impacts of KCNQ1OT1 on cell viability and migration as well as the suppressive impact of KCNQ1OT1 on ECM degradation were partially abolished by miR-126-5p overexpression or TRPS1 knockdown in CHON-001 cells. Conclusions Overexpression of KCNQ1OT1 attenuates the development of OA by sponging miR-126-5p to target TRPS1. Our findings may provide a possible therapeutic strategy for human OA in clinic. |
| first_indexed | 2024-12-22T00:54:42Z |
| format | Article |
| id | doaj.art-cf2ce3f7726c42cf82dad630f195febe |
| institution | Directory Open Access Journal |
| issn | 2523-3106 |
| language | English |
| last_indexed | 2024-12-22T00:54:42Z |
| publishDate | 2021-06-01 |
| publisher | BMC |
| record_format | Article |
| series | Advances in Rheumatology |
| spelling | doaj.art-cf2ce3f7726c42cf82dad630f195febe2022-12-21T18:44:20ZengBMCAdvances in Rheumatology2523-31062021-06-0161111110.1186/s42358-021-00187-3Long non-coding RNA KCNQ1OT1 promotes cell viability and migration as well as inhibiting degradation of CHON-001 cells by regulating miR-126-5p/TRPS1 axisBinfeng Wang0Xiangwei Liu1Orthopaedic Ward 2 (Trauma Surgery), Chifeng Municipal HospitalOrthopaedic Ward 2 (Trauma Surgery), Chifeng Municipal HospitalAbstract Background Osteoarthritis (OA) is defined as a degenerative disease. Pivotal roles of long non-coding RNA (lncRNAs) in OA are widely elucidated. Herein, we intend to explore the function and molecular mechanism of lncRNA KCNQ1OT1 in CHON-001 cells. Methods Relative expression of KCNQ1OT1, miR-126-5p and TRPS1 was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability was examined by MTT assay. The migratory ability of chondrocytes was assessed by transwell assay. Western blot was used to determine relative protein expression of collagen II, MMP13 and TRPS1. Dual-luciferase reporter (DLR) assay was applied to test the target of lncRNA KCNQ1OT1 or miR-126-5p. Results Relative expression of KCNQ1OT1 and TRPS1 was reduced, whereas miR-126-5p was augmented in cartilage tissues of post-traumatic OA patients compared to those of subjects without post-traumatic OA. Increased KCNQ1OT1 or decreased miR-126-5p enhanced cell viability and migration, and repressed extracellular matrix (ECM) degradation in CHON-001 cells. MiR-126-5p was the downstream target of KCNQ1OT1, and it could directly target TRPS1. There was an inverse correlation between KCNQ1OT1 and miR-126-5p or between miR-126-5p and TRPS1. Meantime, there was a positive correlation between KCNQ1OT1 and TRPS1. The promoting impacts of KCNQ1OT1 on cell viability and migration as well as the suppressive impact of KCNQ1OT1 on ECM degradation were partially abolished by miR-126-5p overexpression or TRPS1 knockdown in CHON-001 cells. Conclusions Overexpression of KCNQ1OT1 attenuates the development of OA by sponging miR-126-5p to target TRPS1. Our findings may provide a possible therapeutic strategy for human OA in clinic.https://doi.org/10.1186/s42358-021-00187-3Post-traumatic osteoarthritisKCNQ1 overlapping transcript 1miR-126-5pTricho-rhino-phalangeal syndrome type I |
| spellingShingle | Binfeng Wang Xiangwei Liu Long non-coding RNA KCNQ1OT1 promotes cell viability and migration as well as inhibiting degradation of CHON-001 cells by regulating miR-126-5p/TRPS1 axis Advances in Rheumatology Post-traumatic osteoarthritis KCNQ1 overlapping transcript 1 miR-126-5p Tricho-rhino-phalangeal syndrome type I |
| title | Long non-coding RNA KCNQ1OT1 promotes cell viability and migration as well as inhibiting degradation of CHON-001 cells by regulating miR-126-5p/TRPS1 axis |
| title_full | Long non-coding RNA KCNQ1OT1 promotes cell viability and migration as well as inhibiting degradation of CHON-001 cells by regulating miR-126-5p/TRPS1 axis |
| title_fullStr | Long non-coding RNA KCNQ1OT1 promotes cell viability and migration as well as inhibiting degradation of CHON-001 cells by regulating miR-126-5p/TRPS1 axis |
| title_full_unstemmed | Long non-coding RNA KCNQ1OT1 promotes cell viability and migration as well as inhibiting degradation of CHON-001 cells by regulating miR-126-5p/TRPS1 axis |
| title_short | Long non-coding RNA KCNQ1OT1 promotes cell viability and migration as well as inhibiting degradation of CHON-001 cells by regulating miR-126-5p/TRPS1 axis |
| title_sort | long non coding rna kcnq1ot1 promotes cell viability and migration as well as inhibiting degradation of chon 001 cells by regulating mir 126 5p trps1 axis |
| topic | Post-traumatic osteoarthritis KCNQ1 overlapping transcript 1 miR-126-5p Tricho-rhino-phalangeal syndrome type I |
| url | https://doi.org/10.1186/s42358-021-00187-3 |
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