LncRNA ANCR is positively correlated with transforming growth factor‐β1 in patients with osteoarthritis

Li, Qingsong; Zhang, Zhenxiang; Guo, Shuguang; Tang, Genlin; Lu, Wei; Qi, Xiaojun

doi:10.1002/jcb.28881

Cited by 16 publications

(8 citation statements)

References 21 publications

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“…OA is the most common joint disease with high morbidity in the middle-aged and elderly population [25,26]. Numerous lncRNAs have been confirmed to be downregulated in OA [27][28][29], such as lncRNA ATB [27], lncRNA PACER [28], and lncRNA ANCR [29]. In line with the previous studies, a decreased expression of Fig.…”

Section: Discussionsupporting

confidence: 81%

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

Wang

Liu

2021

Adv Rheumatol

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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.

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Section: Discussionsupporting

confidence: 81%

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

Wang

Liu

2021

Adv Rheumatol

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“…Furthermore, it is a leading cause of disability and shortening of an adult working life globally (26). Numerous lncRNAs have been associated with the development of OA (27)(28)(29). For example, lncRNA anti-differentiation non-coding RNA expression was increased in plasma specimens from patients with OA and CHON-001 human chondrocytes (27).…”

Section: Discussionmentioning

confidence: 99%

“…Numerous lncRNAs have been associated with the development of OA (27)(28)(29). For example, lncRNA anti-differentiation non-coding RNA expression was increased in plasma specimens from patients with OA and CHON-001 human chondrocytes (27). The mRNA expression level of lncRNA MALAT1 was increased in OA tissues and in a time-dependent manner in IL-1β-induced chondrocytes (28).…”

Section: Discussionmentioning

confidence: 99%

Knockdown of LINC01385 inhibits osteoarthritis progression by modulating the microRNA‑140‑3p/TLR4 axis

et al. 2021

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Long non-coding (lnc) RNAs have been associated with osteoarthritis (OA) progression. The aim of the present study was to investigate the regulatory mechanism of lncRNA LINC01385 in OA in vitro. The mRNA expression level of LINC01385, microRNA(miR)-140-3p, and Toll-like receptor 4 (TLR4) was detected using reverse transcription-quantitative PCR, while ELISA was used to determine the concentration of different inflammatory factors [tumor necrosis factor-α (TNF-α), IL-6, and prostaglandin E 2 (PGE 2 )]. The viability of human articular chondrocytes (HC-a) was measured using a MTT assay and western blot analysis was performed to quantify the protein expression level of TLR4. The associations between miR-140-3p and LINC01385/TLR4 were confirmed using a dual-luciferase reporter assay. LINC01385 mRNA expression level was increased in OA tissues and IL-1β-induced HC-a. LINC01385 knockdown and miR-140-3p mimics reduced the concentration of inflammatory factors in IL-1β-induced HC-a and promoted cell survival. In addition, it was confirmed that LINC01385 targeted miR-140-3p, while TLR4 was a target gene of miR-140-3p. Negative correlations between LINC01385 and miR-140-3p, and between miR-140-3p and TLR4 were observed in OA tissues. Low mRNA expression level of miR-140-3p and high protein expression level of TLR4 reversed the inhibitory effect of LINC01385 knockdown on the inflammatory responses of IL-1β-induced HC-a and exhibited a stimulating effect on cell viability. LINC01385 knockdown reduced the progression of OA by modulating the miR-140-3p/TLR4 axis in vitro; thus, LINC01385 may be a therapeutic target for OA.

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“…Previous studies determined that chondrocyte survival was associated with joint destruction in OA patients [21,22]. The human chondrocyte cell line CHON-001, derived from normal human articular cartilage, has been widely used in vitro in osteoarthritis models [23][24][25]. Although researches have been conducted on different aspects of OA, further studies are required to be carried out on the molecular mechanisms involved in chondrocyte survival in OA.…”

Section: Discussionmentioning

confidence: 99%

LncRNA DNM3OS promotes proliferation and inhibits apoptosis through modulating IGF1 expression by sponging MiR-126 in CHON-001 cells

2019

Diagn Pathol

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Background: As a degenerative disease, osteoarthritis (OA) greatly affects aged population. The human chondrocyte cell line CHON-001, derived from normal human articular cartilage, has been widely used in vitro in osteoarthritis models. In order to better understand the underlying mechanism of OA pathogenesis, this study was conducted to explore the effects of LncRNA dynamin 3 opposite strand (DNM3OS) on CHON-001 cells. Methods: The expression levels of and correlation between DNM3OS and miR-126 that derived from OA and non-OA tissues were determined by quantitative real time (qRT)-PCR and Spearman's correlation analysis. Cell viability, clone, migration, invasion and apoptosis were respectively determined by cell counting kit-8, colony formation, wound healing assay, transwell and flow cytometry. The target genes were predicted by starbase V2 and targetscan 7.2 and confirmed by luciferase reporter assay. The expressions of apoptosis-related factors were detected by Western blot. Results: The expression of DNM3OS was down-regulated in OA patients. Functional assays demonstrated that ectopic expression of DNM3OS promoted the proliferation and inhibited apoptosis of CHON-001 cells, and that knocking down DNM3OS suppressed cell proliferation and induced apoptosis. Mechanistic investigation revealed that DNM3OS physically bound to the promoter of miR-126 and suppressed miR-126 expression. Decreased expression of DNM3OS was negatively correlated with miR-126 in OA patients. Furthermore, the effects of siDNM3OS on inhibiting cell proliferation and promoting apoptosis were partially reversed by miR-126 inhibitor. Meanwhile, type insulin-like growth factor-1 (IGF1) was identified as a target gene for miR-126 and was negatively associated with the miR-126 expression. Overexpressed IGF1 restored the effects of miR-126 mimic in suppressing cell proliferation and promoting apoptosis. Conclusion: Our results showed that DNM3OS could affect the CHON-001 cell proliferation and apoptosis by regulating IGF1 by sponging miR-126.

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LncRNA ANCR is positively correlated with transforming growth factor‐β1 in patients with osteoarthritis

Cited by 16 publications

References 21 publications

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

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

Knockdown of LINC01385 inhibits osteoarthritis progression by modulating the microRNA‑140‑3p/TLR4 axis

LncRNA DNM3OS promotes proliferation and inhibits apoptosis through modulating IGF1 expression by sponging MiR-126 in CHON-001 cells

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