scholarly journals Knockdown of long noncoding RNA HOTAIR inhibits osteoarthritis chondrocyte injury by miR-107/CXCL12 axis

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Jipeng Lu ◽  
Zhongxiong Wu ◽  
Ying Xiong
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Cell Apoptosis ◽  
Noncoding Rna ◽  
Underlying Mechanism ◽  
Joint Disease ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Cxcl12 Expression ◽  
Ecm Degradation

Abstract Background Osteoarthritis (OA) is a joint disease characterized via destruction of cartilage. Chondrocyte damage is associated with cartilage destruction during OA. Long noncoding RNAs (lncRNAs) are implicated in the regulation of chondrocyte damage in OA progression. This study aims to investigate the role and underlying mechanism of lncRNA homeobox antisense intergenic RNA (HOTAIR) in OA chondrocyte injury. Methods Twenty-three OA patients and healthy controls without OA were recruited. Chondrocytes were isolated from OA cartilage tissues. HOTAIR, microRNA-107 (miR-107) and C-X-C motif chemokine ligand 12 (CXCL12) levels were measured by quantitative real-time polymerase chain reaction and western blot. Cell proliferation, apoptosis and extracellular matrix (ECM) degradation were measured using cell counting kit-8, flow cytometry and western blot. The target interaction was explored by bioinformatics, luciferase reporter and RNA immunoprecipitation assays. Results HOTAIR expression was enhanced, and miR-107 level was reduced in OA cartilage samples. HOTAIR overexpression inhibited cell proliferation, but induced cell apoptosis and ECM degradation in chondrocytes. HOTAIR knockdown caused an opposite effect. MiR-107 was sponged and inhibited via HOTAIR, and knockdown of miR-107 mitigated the effect of HOTAIR silence on chondrocyte injury. CXCL12 was targeted by miR-107. CXCL12 overexpression attenuated the roles of miR-107 overexpression or HOTAIR knockdown in the proliferation, apoptosis and ECM degradation. CXCL12 expression was decreased by HOTAIR silence, and restored by knockdown of miR-107. Conclusion HOTAIR knockdown promoted chondrocyte proliferation, but inhibited cell apoptosis and ECM degradation in OA chondrocytes by regulating the miR-107/CXCL12 axis.

scholarly journals MEG3 inhibits proliferation and promote apoptosis in osteoarthritis chondrocytes by miR-361-5p/wnt/β-catenin axis

2019 ◽  
Author(s):  
Anying Wang ◽  
Naixia Hu ◽  
Yefeng Zhang ◽  
Yuanzhen Chen ◽  
Changhui Su ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Rat Model ◽  
Cell Apoptosis ◽  
Noncoding Rna ◽  
Molecular Mechanisms ◽  
Luciferase Reporter ◽  
Control Group ◽  
Oa Chondrocytes ◽  
Inhibit Cell Proliferation

Abstract Background: This study aimed to investigate the role of long noncoding RNA (lncRNA) maternally expressed 3 (MEG3) and related molecular mechanisms in osteoarthritis (OA). Methods: Patients with OA and patients undergoing thigh amputation were involved in OA group and control group, respectively. Cartilage tissues of all patients were isolated and cultured. Based on different transfection, MEG3 cells were grouped into Blank, pcDNA3.1-NC, pcDNA3.1-MEG3, si-NC, si-MEG3, pcDNA3.1-NC + mimics NC, pcDNA3.1-MEG3 + mimics NC, pcDNA3.1-NC + miR-361-5p mimics and pcDNA3.1-MEG3 + miR-361-5p mimics group. The cells transfected with pcDNA3.1-NC and pcDNA3.1-MEG3, and then cultured with XAV939 was named as pcDNA3.1-NC +XAV939 group and pcDNA3.1-MEG3 + XAV939 group respectively. The RT-qPCR was used to detect the expression of MEG3 and miR-361-5p. Moreover, Western blot, luciferase reporter assay, RIP, CCK-8 and flow cytometry analysis were performed to reveal the morphology, proliferation and apoptosis in cartilage cells. Finally, the histological analysis and immunostaining were performed on OA rat model. Results: The expression of lncRNA MEG3 and miR-361-5p in OA was significantly decreased and increased respectively than that in normal. Meanwhile, MEG3 was competitive binding with miR-361-5p in OA chondrocytes. Moreover, the Western blot and CCK-8 assay showed that MEG3 might inhibit cell proliferation and promote cell apoptosis via Wnt/β-catenin pathway. Finally, rat model analysis showed that MEG3 contributed to the cartilage matrix degradation. Conclusion: MEG3 and miR-361-5p might down-regulated and up-regulated respectively in the chondrocytes of OA patients. Furthermore, MEG3 might inhibit cell proliferation and promote cell apoptosis via miR-361-5p/Wnt/β-catenin axis in OA chondrocytes.

scholarly journals MEG3 inhibits proliferation and promote apoptosis in osteoarthritis chondrocytes by miR-361-5p/wnt/β-catenin axis

2019 ◽  
Author(s):  
Anying Wang ◽  
Naixia Hu ◽  
Yefeng Zhang ◽  
Yuanzhen Chen ◽  
Changhui Su ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Rat Model ◽  
Cell Apoptosis ◽  
Noncoding Rna ◽  
Molecular Mechanisms ◽  
Luciferase Reporter ◽  
Control Group ◽  
Oa Chondrocytes ◽  
Inhibit Cell Proliferation

Abstract Background: This study aimed to investigate the role of long noncoding RNA (lncRNA) maternally expressed 3 (MEG3) and related molecular mechanisms in osteoarthritis (OA). Methods: Patients with OA and patients undergoing thigh amputation were involved in OA group and control group, respectively. Cartilage tissues of all patients were isolated and cultured. Based on different transfection, MEG3 cells were grouped into Blank, pcDNA3.1-NC, pcDNA3.1-MEG3, si-NC, si-MEG3, pcDNA3.1-NC + mimics NC, pcDNA3.1-MEG3 + mimics NC, pcDNA3.1-NC + miR-361-5p mimics and pcDNA3.1-MEG3 + miR-361-5p mimics group. The cells transfected with pcDNA3.1-NC and pcDNA3.1-MEG3, and then cultured with XAV939 was named as pcDNA3.1-NC +XAV939 group and pcDNA3.1-MEG3 + XAV939 group respectively. The RT-qPCR was used to detect the expression of MEG3 and miR-361-5p . Moreover, Western blot, luciferase reporter assay, RIP, CCK-8 and flow cytometry analysis were performed to reveal the morphology, proliferation and apoptosis in cartilage cells. Finally, the histological analysis and immunostaining were performed on OA rat model. Results: The expression of lncRNA MEG3 and miR-361-5p in OA was significantly decreased and increased respectively than that in normal. Meanwhile, MEG3 was competitive binding with miR-361-5p in OA chondrocytes. Moreover, the Western blot and CCK-8 assay showed that MEG3 might inhibit cell proliferation and promote cell apoptosis via Wnt/β-catenin pathway. Finally, rat model analysis showed that MEG3 contributed to the cartilage matrix degradation. Conclusion: MEG3 and miR-361-5p might down-regulated and up-regulated respectively in the chondrocytes of OA patients. Furthermore, MEG3 might inhibit cell proliferation and promote cell apoptosis via miR-361-5p/Wnt/β-catenin axis in OA chondrocytes.

scholarly journals Long noncoding RNA TUG1 regulates degradation of chondrocyte extracellular matrix via miR-320c/MMP-13 axis in osteoarthritis

2021 ◽  
Vol 16 (1) ◽  
pp. 384-394
Author(s):  
Hu Han ◽  
Lijuan Liu
Keyword(s):  
Extracellular Matrix ◽  
Cell Proliferation ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Joint Disease ◽  
Luciferase Reporter ◽  
Rna Immunoprecipitation ◽  
Ecm Degradation ◽  
Polymerase Chain ◽  
Insight Into

Abstract Osteoarthritis (OA) is a common chronic joint disease. This study aimed to explore the function of long noncoding RNA taurine-upregulated gene 1 (TUG1) in the progression and initiation of OA. Levels of TUG1, microRNA-320c (miR-320c) and fucosyltransferase 4 (FUT4) were examined via quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide and flow cytometry assays were used to detect cell viability and apoptosis, respectively. The expression of relative proteins was measured using Western blot. The interaction between miR-320c and TUG1 or FUT4 was confirmed utilizing dual-luciferase reporter and RNA immunoprecipitation assays. In this study, levels of TUG1 and FUT4 were distinctly upregulated, but miR-320c level significantly decreased in OA tissues and chondrocytes derived from OA tissues as well as in IL-1β-stimulated C28/I2 cells. Mechanically, TUG1 sponged miR-320c and miR-320c targeted FUT4. In addition, TUG1 knockdown accelerated cell proliferation and repressed apoptosis and extracellular matrix (ECM) degradation in IL-1β-induced C28/I2 cells, whereas these effects of TUG1 deletion were rescued by either miR-320c inhibitor or FUT4 upregulation. Meanwhile, TUG1 sponged miR-320c to regulate FUT4 expression in IL-1β-induced C28/I2 cells. Collectively, TUG1 modulated cell proliferation, apoptosis and ECM degradation in IL-1β-induced C28/I2 cells via the miR-320c/FUT4 axis, providing a new insight into the OA treatment.

scholarly journals MEG3 inhibits proliferation and promote apoptosis in osteoarthritis chondrocytes by miR-361-5p/wnt/β-catenin axis

2019 ◽  
Author(s):  
Anying Wang ◽  
Naixia Hu ◽  
Yefeng Zhang ◽  
Yuanzhen Chen ◽  
Changhui Su ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Rat Model ◽  
Cell Apoptosis ◽  
Noncoding Rna ◽  
Molecular Mechanisms ◽  
Luciferase Reporter ◽  
Control Group ◽  
Oa Chondrocytes ◽  
Inhibit Cell Proliferation

Abstract Background: This study aimed to investigate the role of long noncoding RNA (lncRNA) maternally expressed 3 (MEG3) and related molecular mechanisms in osteoarthritis (OA). Methods: Patients with OA and patients undergoing thigh amputation were involved in OA group and control group, respectively. Cartilage tissues of all patients were isolated and cultured. Based on different transfection, MEG3 cells were grouped into Blank, pcDNA3.1-NC, pcDNA3.1-MEG3, si-NC, si-MEG3, pcDNA3.1-NC + mimics NC, pcDNA3.1-MEG3 + mimics NC, pcDNA3.1-NC + miR-361-5p mimics and pcDNA3.1-MEG3 + miR-361-5p mimics group. The cells transfected with pcDNA3.1-NC and pcDNA3.1-MEG3, and then cultured with XAV939 was named as pcDNA3.1-NC +XAV939 group and pcDNA3.1-MEG3 + XAV939 group respectively. The RT-qPCR was used to detect the expression of MEG3 and miR-361-5p. Moreover, Western blot, luciferase reporter assay, RIP, CCK-8 and flow cytometry analysis were performed to reveal the morphology, proliferation and apoptosis in cartilage cells. Finally, the histological analysis and immunostaining were performed on OA rat model. Results: The expression of lncRNA MEG3 and miR-361-5p in OA was significantly decreased and increased respectively than that in normal. Meanwhile, MEG3 was competitive binding with miR-361-5p in OA chondrocytes. Moreover, the Western blot and CCK-8 assay showed that MEG3 might inhibit cell proliferation and promote cell apoptosis via Wnt/β-catenin pathway. Finally, rat model analysis showed that MEG3 contributed to the cartilage matrix degradation. Conclusion: MEG3 and miR-361-5p might down-regulated and up-regulated respectively in the chondrocytes of OA patients. Furthermore, MEG3 might inhibit cell proliferation and promote cell apoptosis via miR-361-5p/Wnt/β-catenin axis in OA chondrocytes.

scholarly journals NEAT1 aggravates sepsis-induced acute kidney injury by sponging miR-22-3p

Open Medicine ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. 333-342
Author(s):  
Yawei Feng ◽  
Jun Liu ◽  
Ranliang Wu ◽  
Peng Yang ◽  
Zhiqiang Ye ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Western Blot ◽  
Cell Apoptosis ◽  
Noncoding Rna ◽  
Cell Injury ◽  
Kidney Injury ◽  
Inflammatory Factors ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Western Blot Assay

AbstractBackground and aimAcute kidney injury (AKI) is a common complication of sepsis. Long noncoding RNA nuclear-enriched abundant transcript 1 (NEAT1) plays a vital role in various diseases, including AKI. This study aimed to investigate the function and mechanism of NEAT1 in sepsis-induced AKI.Materials and methodsA septic AKI model was established by treating HK-2 cells with lipopolysaccharide (LPS). The levels of NEAT1 and miR-22-3p were measured by quantitative real-time PCR. Cell apoptosis was assessed by flow cytometry. The levels of apoptosis-related protein and autophagy-related factors were examined by the western blot assay. An enzyme-linked immunosorbent assay was used to calculate the contents of inflammatory factors. The interaction between NEAT1 and miR-22-3p was validated by dual-luciferase reporter assay, RNA immunoprecipitation assay, and RNA pull-down assay. The levels of nuclear factor (NF)-κB pathway-related proteins were evaluated by the western blot assay.ResultsNEAT1 was upregulated, while miR-22-3p was downregulated in patients with sepsis and in LPS-stimulated HK-2 cells. LPS treatment triggered cell apoptosis, autophagy, and inflammatory response in HK-2 cells. NEAT1 knockdown attenuated LPS-induced cell injury. NEAT1 modulated LPS-triggered cell injury by targeting miR-22-3p. Furthermore, NEAT1 regulated the NF-κB pathway by modulating miR-22-3p.ConclusionDepletion of NEAT1 alleviated sepsis-induced AKI via regulating the miR-22-3p/NF-κB pathway.

scholarly journals Long Noncoding RNA XIST Promotes Osteosarcoma Progression by Targeting Ras-Related Protein RAP2B via miR-320b

2018 ◽  
Vol 26 (6) ◽  
pp. 837-846 ◽  
Author(s):  
Gong-Yi Lv ◽  
Jun Miao ◽  
Xiao-Lin Zhang
Keyword(s):  
Cell Proliferation ◽  
Noncoding Rna ◽  
Prognostic Biomarker ◽  
Underlying Mechanism ◽  
Luciferase Reporter ◽  
Related Protein ◽  
Xist Expression ◽  
Lncrna Xist ◽  
Proliferation And Invasion ◽  
Invasion Assays

Abnormal expression of long noncoding RNAs (lncRNAs) often contributes to the unrestricted growth and invasion of cancer cells. lncRNA X-inactive specific transcript (XIST) expression is upregulated in several cancers; however, its underlying mechanism in osteosarcoma (OS) has not been elucidated. In the present study, we found that XIST expression was significantly increased in OS tissues and cell lines by LncRNA Profiler and qRT-PCR. The effects of XIST and miR-320b on OS cell proliferation and invasion were studied by MTT and Transwell invasion assays. The competing relationship between XIST and miR-320b was confirmed by luciferase reporter assay. Our results showed that XIST knockdown strikingly inhibited cell proliferation and invasion. Furthermore, XIST could directly bind to miR-320b and repress miR-320b expression. Moreover, XIST overexpression significantly relieved the inhibition on OS cell proliferation and invasion mediated by miR-320b overexpression, which involved the derepression of Ras-related protein RAP2B. We propose that XIST is responsible for OS cell proliferation and invasion and that XIST exerts its function through the miR-320b/RAP2B axis. Our findings suggest that lncRNA XIST may be a candidate prognostic biomarker and a target for new therapies in OS patients.

scholarly journals MEG3 promotes proliferation and inhibits apoptosis in osteoarthritis chondrocytes by miR-361-5p/FOXO1 axis

2019 ◽  
Author(s):  
Anying Wang ◽  
Naixia Hu ◽  
Yefeng Zhang ◽  
Yuanzhen Chen ◽  
Changhui Su ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Cell Apoptosis ◽  
Molecular Mechanisms ◽  
Luciferase Reporter ◽  
Non Coding Rna ◽  
Cartilage Cells ◽  
Osteoarthritis Chondrocytes ◽  
Oa Chondrocytes

Abstract Background: This study aimed to investigate the role of long non-coding RNA (lncRNA) maternally expressed 3 (MEG3) and related molecular mechanisms, in osteoarthritis (OA). Methods: Cartilage tissues of OA patients and healthy volunteers were isolated and cultured. After transfection with the appropriate construct, chondrocytes were classified into Blank, pcDNA3.1-NC, pcDNA3.1-MEG3, si-NC, si-MEG3, pcDNA3.1-NC + mimics NC, pcDNA3.1-MEG3 + mimics NC, pcDNA3.1-NC + miR-361-5p mimics and pcDNA3.1-MEG3 + miR-361-5p mimics groups. qRT-PCR was used to detect the expression of MEG3, miR-361-5p and FOXO1 . Western blot, luciferase reporter assay, RIP, CCK-8, and flow cytometry analysis were performed to reveal the morphology, proliferation, and apoptotic status of cartilage cells. Histological analysis and immunostaining were conducted in the OA rat model. Results: Expression of MEG3 and FOXO1 was significantly decreased in OA compared with the normal group, while the expression of miR-361-5p was increased. MEG3 might serve as a ceRNA of miR-361-5p in OA chondrocytes. Moreover, using western blot analyses and the CCK-8 assay, MEG3 was shown to target miR-361-5p/FOXO1, elevate cell proliferation, and impair cell apoptosis. Functional analysis in vivo showed that MEG3 suppressed degradation of the cartilage matrix. Conclusion: MEG3 can contribute to cell proliferation and inhibit cell apoptosis and degradation of extracellular matrix (ECM) via the miR-361-5p/FOXO1 axis in OA chondrocytes.

scholarly journals Long noncoding RNA-MEG3 contributes to myocardial ischemia–reperfusion injury through suppression of miR-7-5p expression

2019 ◽  
Vol 39 (8) ◽  
Author(s):  
Liyuan Zou ◽  
Xiaokun Ma ◽  
Shuo Lin ◽  
Bingyuan Wu ◽  
Yang Chen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Caspase 3 ◽  
Ischemia Reperfusion Injury ◽  
Cell Model ◽  
Ischemia Reperfusion ◽  
Luciferase Reporter

Abstract Long noncoding RNA (lncRNA) maternally expressed gene 3 (MEG3) plays an important role in protection of ischemia–reperfusion (I/R) injury in brain and liver. However, role of MEG3 in myocardial I/R injury remains unclear. Here, the role of MEG3 in protection of myocardial I/R injury and its association with microRNA-7-5p (miR-7-5p) was investigated using rat cardiac I/R model and myocardial I/R cell model. Our results showed that MEG3 was significantly up-regulated and miR-7-5p was significantly down-regulated after I/R. Following I/R, the levels of intact PARP and intact caspase-3 were reduced, while the cleaved fragments of PARP and caspase-3 were increased. TUNEL assay showed an increase in cardiomyocyte apoptosis after I/R. The levels of I/R-induced creatine kinase (CK) and lactate dehydrogenase (LDH) were inhibited by knockdown of MEG3 (siMEG3). SiMEG3 increased cell proliferation and inhibited cell apoptosis after I/R. In contrast, overexpression of MEG3 increased the I/R-induced CK and LDH activities and cell apoptosis and decreased cell proliferation. The dual-luciferase reporter system showed a direct binding of MEG3 to miR-7-5p. The level of miR-7-5p was negatively associated with the change in levels of MEG3 in H9c2 cells. The levels of intact RARP1 and caspase-3 were significantly increased by knockdown of MEG3. Co-transfection of miR-7-5p inhibitor with siMEG3 activates CK and LDH, significantly decreased cell proliferation, increased cell apoptosis, and decreased intact poly(ADP-ribose) polymerase 1 (PARP1) and caspase-3. In summary, down-regulation of MEG3 protects myocardial cells against I/R-induced apoptosis through miR-7-5p/PARP1 pathway, which might provide a new therapeutic target for treatment of myocardial I/R injury.

scholarly journals Long noncoding RNA UCA1 facilitates cell proliferation and inhibits apoptosis via activating PI3K/Akt pathway in retinoblastoma

2019 ◽  
Author(s):  
Zhongfang Yuan ◽  
Zhaona Li
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Noncoding Rna ◽  
Cell Counting ◽  
Akt Pathway ◽  
Promote Cell Proliferation ◽  
Cell Clones ◽  
Y79 Cells ◽  
The Relationship

Abstract Background This study aimed to explored the effect of lncRNA-UCA1 on retinoblastoma (RB) and its potential molecular mechanisms.Methods In our study, the expression of lncRNA-UCA1 was measured by qRT-RCR in both RB tissues and RB HXO-RB44 and Y79 cells. The relationship between lncRNA-UCA1 expression and clinical parameters in RB patients were evaluated. Cell proliferation, cell clones, apoptosis and cell cycle of HXO-RB44 and Y79 cells were measured by cell counting kit-8 (CCK-8) assay, colony formation assay and flow cytometry, respectively. In addition, the expressions of PCNA, Caspase-3, survivin, p16, p21, CDK2, PI3K, p-PI3K, Akt, p-Akt and S6k in HXO-RB44 and Y79 cells were measured by western blot.Results lncRNA-UCA1 was highly expressed in both RB tissues and RB HXO-RB44 and Y79 cells. Moreover, the expression of lncRNA-UCA1 in RB patients was remarkedly correlated with tumor size, optic nerve invasion and pathologic grade. lncRNA-UCA1 markedly facilitated cell proliferation and cell cycle procession, as well as inhibited cell apoptosis in HXO-RB44 and Y79 cells. lncRNA-UCA1 dramatically increased the expression of S6k and the phosphorylation of PI3K and Akt in RB cells. LY294002 (PI3K inhibitor) reversed the effects of lncRNA-UCA1 on RB cell proliferation, apoptosis and cell cycle procession.Conclusions Our study indicated that lncRNA-UCA1 could promote cell proliferation and cell cycle procession, as well as inhibit cell apoptosis in RB via activating PI3K/Akt pathway.

scholarly journals Long Noncoding RNA MALAT1 Interacts with miR-124-3p to Modulate Osteosarcoma Progression by Targeting SphK1

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Bin Liu ◽  
Xinli Zhan ◽  
Chong Liu
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
Noncoding Rna ◽  
Underlying Mechanism ◽  
Luciferase Reporter ◽  
Cell Proliferation And Migration ◽  
Lncrna Malat1 ◽  
And Migration ◽  
Tissue Specimens ◽  
Proliferation And Migration

Introduction. Long noncoding RNAs (lncRNAs) have been implicated in a variety of biological functions, including tumor proliferation, apoptosis, progression, and metastasis. lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is overexpressed in various cancers, as well as osteosarcoma (OS); however, its underlying mechanism in OS is poorly understood. This investigation aims to elucidate the mechanisms of MALAT1 in OS proliferation and migration and to provide theoretical grounding for further targeted therapy in OS. Methods. In the present study, we applied qRT-PCR to assess the MALAT1 expression in OS tissues and cell lines. The effects of MALAT1 and miR-124-3p on OS cell proliferation and migration were studied by CCK-8 and scratch assays. Cell cycle and apoptosis were tested using a flow cytometer. The competing relationship between MALAT1 and miR-124-3p was confirmed by dual-luciferase reporter assay. Results. MALAT1 was overexpressed in OS cell lines and tissue specimens, and knockdown of MALAT1 significantly inhibited cell proliferation and migration and increased cell apoptosis and the percentage of G0/G1 phase. Furthermore, MALAT1 could directly bind to miR-124-3p and inhibit miR-124-3p expression. Moreover, MALAT1 overexpression significantly relieved the inhibition on OS cell proliferation mediated by miR-124-3p overexpression, which involved the derepression of sphingosine kinase 1 (SphK1). Conclusions. We propose that lncRNA MALAT1 interacts with miR-124-3p to modulate OS progression by targeting SphK1. Hence, we identified a novel MALAT1/miR-124-3p/SphK1 signaling pathway in the regulation of OS biological behaviors.

Sign in / Sign up

Export Citation Format

Share Document