lncRNA‐CIR regulates cell apoptosis of chondrocytes in osteoarthritis

Lu, Zekai; Luo, Min; Huang, Yongpan

doi:10.1002/jcb.27997

Cited by 24 publications

(14 citation statements)

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“…Detailedly, the study elucidated that the amplification of lncRNA-CIR could increase the viability as well as invasion of bladder cancer cells [12]. What’s more, a recent document has pointed out that the reduction of lncRNA-CIR was able to inhibit apoptosis of chondrocytes in OA [19], and Li et al [10] have discovered that lncRNA-CIR could contribute to the degradation of chondrocyte extracellular matrix in OA. Except for cellular experiments, we have also conducted subcutaneous tumorigenesis in nude mice to observe the effect of lncRNA-CIR on osteosarcoma tumor growth in vivo, which has revealed that the suppression of lncRNA-CIR has the ability to restrain tumor growth in nude mice that had been injected with osteosarcoma cells, while the overexpressed lncRNA-CIR exerted an opposite impact.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Degradation of long non-coding RNA-CIR decelerates proliferation, invasion and migration, but promotes apoptosis of osteosarcoma cells

Liu

Kang

et al. 2019

Cancer Cell Int

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BackgroundOver the years, long non-coding RNAs (lncRNAs) have been clarified in malignancies, this research was focused on the role of lncRNA cartilage injury-related (lncRNA-CIR) in osteosarcoma cells.MethodsLncRNA-CIR expression in osteosarcoma tissues and cells, and adjacent normal tissues and normal osteoblasts was determined, then the relations between lncRNA-CIR expression and the clinicopathological features, and between lncRNA-CIR expression and the prognosis of osteosarcoma patients were analyzed. Moreover, the MG63 and 143B cells were treated with silenced or overexpressed lncRNA-CIR, and then the proliferation, invasion, migration and apoptosis of the cells were evaluated by gain- and loss-of-function approaches. The tumor growth, and proliferation and apoptosis of osteosarcoma cells in vivo were observed by subcutaneous tumorigenesis in nude mice.ResultsWe have found that lncRNA-CIR was up-regulated in osteosarcoma tissues and cells, which was respectively relative to adjacent normal tissues and normal osteoblasts. The expression of lncRNA-CIR was evidently correlated with disease stages, distant metastasis and differentiation of osteosarcoma patients, and the high expression of lncRNA-CIR indicated a poor prognosis. Furthermore, the reduction of lncRNA-CIR could restrict proliferation, invasion and migration, but promote apoptosis of osteosarcoma cells in vitro. Meanwhile, inhibited lncRNA-CIR also restrained tumor growth and osteosarcoma cell proliferation, whereas accelerated apoptosis of osteosarcoma cells in vivo.ConclusionWe have found in this study that the inhibited lncRNA-CIR could decelerate proliferation, invasion and migration, but accelerate apoptosis of osteosarcoma cells, which may provide a novel target for osteosarcoma treatment.

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Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Degradation of long non-coding RNA-CIR decelerates proliferation, invasion and migration, but promotes apoptosis of osteosarcoma cells

Liu

Kang

et al. 2019

Cancer Cell Int

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“…OA is mainly a disease of the elderly, influencing principally the knees and hips [16]. Recently, a report has shown that changes in the expression levels of lncRNAs have been connected with all kinds of disease processes, including OA [17]. Furthermore, a prior study have noted that excitement of chondrocytes with Wnt-β-catenin has been conveyed to facilitate the expression levels of a variety of elements concerned with OA [18].…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Silencing lncRNA HOTAIR declines synovial inflammation and synoviocyte proliferation and promotes synoviocyte apoptosis in osteoarthritis rats by inhibiting Wnt/β-catenin signaling pathway

Tian

et al. 2019

Cell Cycle

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Osteoarthritis (OA) is a degenerative injury of the articular cartilage and reactive hyperplasia of the articular rim and subchondral bone. Due to its poor prognosis, this study is to research the influences of lncRNA HOTAIR on synovial inflammation and synoviocyte apoptosis and proliferation in OA rats by regulating the Wnt/β-catenin pathway. Rat OA model was constructed by means of cruciate ligament resection, and the successfully modeled rats were injected with sh-HOTAIR, or Wnt/β-catenin pathway activator (LiCl), and synoviocytes were transfected with sh-HOTAIR or LiCl for investigation of the influences of HOTAIR and Wnt/β-catenin pathway on synoviocytes proliferation and apoptosis. ELISA and RT-qPCR were used to detect the levels of IL-1β, IL-6 and TNF-α in serum, synovial tissue and synoviocytes in rats, respectively. The protein levels of bax, bcl-2, wnt1 and β-catenin in synovial tissue and synoviocytes were tested by Western blot analysis. Highly expressed HOTAIR existed in synovial tissue and synoviocytes of rats. There were declining arthritis index, inflammation, synoviocytes proliferation, cycle progression and promoted synoviocytes apoptosis by silencing HOTAIR and inhibited Wnt/β-catenin pathway. Down-regulation of HOTAIR could reverse the effect of LiCl on progression of OA rats. There was strained activation of Wnt/β-catenin pathway via declining HOTAIR. This study suggests that silencing lncRNA HOTAIR and inhibited Wnt/β-catenin pathway decline synovial inflammation and synoviocyte proliferation and promote apoptosis in OA rats.

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“…4-HNE and 8-oxo-dG are well-characterized oxidative damage makers that have been associated to pathological processes like mitochondrial dysfunction, apoptosis, mutagenesis, and inflammation in the joint (Abusarah et al 2017;Biniecka et al 2011a, b;Vaamonde-García et al 2017). Besides, different in vitro studies show that oxidative stress is involved in altered chondrocyte survival (Cheleschi et al 2017;Goutas et al 2018;Lu et al 2018) and act as second messengers in signaling cascades that activate the expression of catabolic mediators such as metalloproteinases like MMP-13 (Del Carlo et al 2007;Gao et al 2018), favoring cartilage degradation. We and other authors have previously described in vitro an antioxidant role of H 2 S in chondrocytes (Burguera et al 2014;Fox et al 2012).…”

Section: Discussionmentioning

confidence: 99%

Effect of balneotherapy in sulfurous water on an in vivo murine model of osteoarthritis

et al. 2019

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Osteoarthritis (OA) is a chronic joint disease that results in progressive cartilage destruction and subsequently joint dysfunction. Growing evidence indicates beneficial impact of balneological interventions in OA; however, their mechanisms of action are still unclear. Here, we evaluate the effect of balneotherapy in sulfurous water in an OA experimental model. Experimental OA was induced in Wistar rats by transection of the medial collateral ligament and removal of the medial meniscus of the left knee. Animals were randomized into three groups: non-treated (control) and balneotherapy using sulfurous water (SW) or tap water (TW). Macroscopic evaluation was performed, as well as evaluation of pain levels and analysis of motor function by rotarod test. Histopathological changes in articular cartilage and synovium were also evaluated. The presence of matrix metalloproteinase-13 (MMP-13) and oxidative damage markers was assessed by immunohistochemistry. Joint destabilization induced joint thickening, loss of joint flexion, and increased levels of pain. At day 40, animals from SW group presented lower pain levels than those from control group. Experimental OA also affected motor function. Balneotherapy in sulfur-rich water significantly improved joint mobility in relation to that in tap water. Besides, we observed that cartilage deterioration was lower in SW group than in the other two groups. Likewise, SW group showed reduced levels of MMP-13 in the cartilage. Conversely, we failed to observe any modulation on synovial inflammation. Finally, balneotherapy in sulfurous water diminished the presence of oxidative damage markers. Our results suggest the beneficial effect of balneotherapy in sulfur-rich water on an experimental model of OA, showing a reduced cartilage destruction and oxidative damage. Thus, these findings support the use of balneotherapy as a non-pharmacological treatment in OA.

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lncRNA‐CIR regulates cell apoptosis of chondrocytes in osteoarthritis

Cited by 24 publications

References 14 publications

RETRACTED ARTICLE: Degradation of long non-coding RNA-CIR decelerates proliferation, invasion and migration, but promotes apoptosis of osteosarcoma cells

RETRACTED ARTICLE: Degradation of long non-coding RNA-CIR decelerates proliferation, invasion and migration, but promotes apoptosis of osteosarcoma cells

RETRACTED ARTICLE: Silencing lncRNA HOTAIR declines synovial inflammation and synoviocyte proliferation and promotes synoviocyte apoptosis in osteoarthritis rats by inhibiting Wnt/β-catenin signaling pathway

Effect of balneotherapy in sulfurous water on an in vivo murine model of osteoarthritis

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