scholarly journals A CREB1-miR-181a-5p loop regulates the pathophysiologic features of bone marrow stromal cells in fibrous dysplasia of bone

2021 ◽  
Vol 27 (1) ◽  
Author(s):  
Yu Fu ◽  
Zhili Xin ◽  
Ziji Ling ◽  
Hanyu Xie ◽  
Tao Xiao ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Fibrous Dysplasia ◽  
Proliferative Activity ◽  
Molecular Mechanisms ◽  
Luciferase Reporter ◽  
Sequencing Analysis ◽  
Guanine Nucleotide Binding Protein ◽  
Activation Effect ◽  
Downstream Target ◽  
Regulatory Loop

Abstract Background Fibrous dysplasia (FD) is a bone marrow stromal cell (BMSC) disease caused by activating mutations of guanine nucleotide-binding protein alpha-stimulating activity polypeptide (GNAS) and is characterized by increased proliferative activity and disrupted osteogenesis of BMSCs. However, the molecular mechanisms regulating the pathophysiologic features of BMSCs in FD remain unknown. This study aimed to identify and verify the roles of the CREB1-miR-181a-5p regulatory loop in FD pathophysiology. Methods MicroRNA (miRNA) sequencing analysis was used to identify the possible miRNAs implicated in FD. The proliferation, apoptosis, and osteogenic differentiation of BMSCs, as well as the osteoclast-induced phenotype, were measured and compared after exogenous miR-181a-5p transfection into FD BMSCs or miR-181a-5p inhibitor transfection into normal BMSCs. Chromatin immunoprecipitation and luciferase reporter assays were performed to verify the interactions between CREB1 and miR-181a-5p and their effects on the FD pathological phenotype. Results Compared to normal BMSCs, FD BMSCs showed decreased miR-181a-5p levels and exhibited increased proliferative activity, decreased apoptotic capacity, and impaired osteogenesis. FD BMSCs also showed a stronger osteoclast activation effect. miR-181a-5p overexpression reversed the pathophysiologic features of FD BMSCs, whereas miR-181a-5p suppression induced an FD-like phenotype in normal BMSCs. Mechanistically, miR-181a-5p was the downstream target of CREB1, and CREB1 was posttranscriptionally regulated by miR-181a-5p. Conclusions Our study identifies that the interaction loop between CREB1 and miR-181a-5p plays a crucial role in regulating the pathophysiologic features of FD BMSCs. MiR-181a-5p may be a potential therapeutic target for the treatment of FD.

scholarly journals Circular RNA AFF4 modulates osteogenic differentiation in BM-MSCs by activating SMAD1/5 pathway through miR-135a-5p/FNDC5/Irisin axis

2021 ◽  
Vol 12 (7) ◽  
Author(s):  
Chao Liu ◽  
An-Song Liu ◽  
Da Zhong ◽  
Cheng-Gong Wang ◽  
Mi Yu ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Formation ◽  
Osteogenic Differentiation ◽  
Molecular Mechanisms ◽  
Expression Patterns ◽  
Regulatory System ◽  
Circular Rna ◽  
Luciferase Reporter ◽  
Integrin Αv

AbstractBone marrow-derived mesenchymal stem cells (BM-MSCs), the common progenitor cells of adipocytes and osteoblasts, have been recognized as the key mediator during bone formation. Herein, our study aim to investigate molecular mechanisms underlying circular RNA (circRNA) AFF4 (circ_AFF4)-regulated BM-MSCs osteogenesis. BM-MSCs were characterized by FACS, ARS, and ALP staining. Expression patterns of circ_AFF4, miR-135a-5p, FNDC5/Irisin, SMAD1/5, and osteogenesis markers, including ALP, BMP4, RUNX2, Spp1, and Colla1 were detected by qRT-PCR, western blot, or immunofluorescence staining, respectively. Interactions between circ_AFF4 and miR-135a-5p, FNDC5, and miR-135a-5p were analyzed using web tools including TargetScan, miRanda, and miRDB, and further confirmed by luciferase reporter assay and RNA pull-down. Complex formation between Irisin and Integrin αV was verified by Co-immunoprecipitation. To further verify the functional role of circ_AFF4 in vivo during bone formation, we conducted animal experiments harboring circ_AFF4 knockdown, and born samples were evaluated by immunohistochemistry, hematoxylin and eosin, and Masson staining. Circ_AFF4 was upregulated upon osteogenic differentiation induction in BM-MSCs, and miR-135a-5p expression declined as differentiation proceeds. Circ_AFF4 knockdown significantly inhibited osteogenesis potential in BM-MSCs. Circ_AFF4 stimulated FNDC5/Irisin expression through complementary binding to its downstream target molecule miR-135a-5p. Irisin formed an intermolecular complex with Integrin αV and activated the SMAD1/5 pathway during osteogenic differentiation. Our work revealed that circ_AFF4, acting as a sponge of miR-135a-5p, triggers the promotion of FNDC5/Irisin via activating the SMAD1/5 pathway to induce osteogenic differentiation in BM-MSCs. These findings gained a deeper insight into the circRNA-miRNA regulatory system in the bone marrow microenvironment and may improve our understanding of bone formation-related diseases at physiological and pathological levels.

scholarly journals MicroRNA-346-5p Regulates Differentiation of Bone Marrow-Derived Mesenchymal Stem Cells by Inhibiting Transmembrane Protein 9

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Yicai Zhang ◽  
Yi Sun ◽  
Jinlong Liu ◽  
Yu Han ◽  
Jinglong Yan
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Osteogenic Differentiation ◽  
Protein Level ◽  
Molecular Mechanisms ◽  
Transmembrane Protein ◽  
Luciferase Reporter ◽  
Alizarin Red ◽  
Protein Levels

The molecular mechanisms how bone marrow-derived mesenchymal stem cells (BMSCs) differentiate into osteoblast need to be investigated. MicroRNAs (miRNAs) contribute to the osteogenic differentiation of BMSCs. However, the effect of miR-346-5p on osteogenic differentiation of BMSCs is not clear. This study is aimed at elucidating the underlying mechanism by which miR-346-5p regulates osteogenic differentiation of human BMSCs. Results of alkaline phosphatase (ALP) and Alizarin Red S (ARS) staining indicated that upregulation of miR-346-5p suppressed osteogenic differentiation of BMSCs, whereas downregulation of miR-346-5p enhanced this process. The protein levels of the osteoblastic markers Osterix and Runt-related transcription factor 2 (Runx2) were decreased in cells treated with miR-346-5p mimic at day 7 and day 14 after being differentiated. By contrast, downregulation of miR-346-5p elevated the protein levels of Osterix and Runx2. Moreover, a dual-luciferase reporter assay revealed that Transmembrane Protein 9 (TMEM9) was a target of miR-346-5p. In addition, the Western Blot results demonstrated that the TMEM9 protein level was significantly reduced by the miR-346-5p mimic whereas downregulation of miR-346-5p improved the protein level of TMEM9. These results together demonstrated that miR-346-5p served a key role in BMSC osteogenic differentiation of through targeting TMEM9, which may provide a novel target for clinical treatments of bone injury.

scholarly journals miR-142-5p in Bone Marrow-Derived Mesenchymal Stem Cells Promotes Osteoporosis Involving Targeting Adhesion Molecule VCAM-1 and Inhibiting Cell Migration

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Zhaowei Teng ◽  
Xueguan Xie ◽  
Yun Zhu ◽  
Jianping Liu ◽  
Xingbo Hu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Adhesion Molecule ◽  
The Elderly ◽  
Luciferase Reporter ◽  
Sequencing Analysis ◽  
Migration Ability ◽  
Aberrant Expression ◽  
Migration Assay

Osteoporosis is a systemic bone metabolic disease that is highly prevalent in the elderly population, particularly in postmenopausal women, which results in enhanced bone fragility and an increased susceptibility to fractures. However, the underlying molecular pathogenesis mechanisms still remain to be further elucidated. In this study, in a rat ovariectomy- (OVX-) induced postmenopausal osteoporosis model, aberrant expression of a microRNA miR-142-5p and vascular cell adhesion molecule 1 (VCAM-1) was found by RNA sequencing analysis and qRT-PCR. Using a dual-luciferase reporter assay, we found that miR-142-5p can bind to and decrease expression of VCAM-1 mRNA. Such reduction was prohibited when the miR-142-5p binding site in VCAM-1 3′UTR was deleted, and Western blotting analyses validated the fact that miR-142-5p inhibited the expression of VCAM-1 protein. Bone marrow-derived mesenchymal stem cells (BMMSCs) transfected with miR-142-5p showed a significantly decreased migration ability in a Transwell migration assay. Collectively, these data indicated the important role of miR-142-5p in osteoporosis development involving targeting VCAM-1 and inhibiting BMMSC migration.

scholarly journals The Long Non-coding RNA TMPO-AS1  Promotes Bladder Cancer Growth and Progression via OTUB1-induced E2F1 Deubiquitination

2020 ◽  
Author(s):  
Yeyu Zhang ◽  
Yuxing Zhu ◽  
Mengqing Xiao ◽  
Yaxin Cheng ◽  
Dong He ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Molecular Mechanisms ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
E2f Transcription Factor ◽  
Rna Immunoprecipitation ◽  
Regulatory Loop

Abstract BackgroundBladder cancer (BC) is the most common malignant tumor of the urinary system. Increasing evidence indicates long non-coding RNAs (lncRNAs) play crucial roles in cancer tumorigenesis, development, and progression. However, the role of TMPO antisense RNA 1 (TMPO-AS1) is still need to be explored in BC.MethodsThe lncRNA TMPO-AS1 expression was evaluated by bioinformatics analysis and further validated by qRT-PCR. Loss- and gain-of- function assays were performed to determine the biological functions of TMPO-AS1 in BC proliferation, migration, and invasion. Chromatin immunoprecipitation, luciferase reporter assays, western blotting, RNA pull-down, RNA immunoprecipitation assays, and fluorescence in situ hybridization were conducted to explore the molecular mechanisms of TMPO-AS1/E2F transcription factor 1 (E2F1) loop. ResultsTMPO-AS1 is upregulated in bladder cancer and is associated with BC patients’ poor prognoses. Functional experiments demonstrated that TMPO-AS1 promotes bladder cancer cell proliferation, migration, invasion, and inhibits cell apoptosis in vivo and in vitro. Mechanically, E2F1 is responsible for the TMPO-AS1 upregulation. Additionally, TMPO-AS1 facilitates the interaction of E2F1 with OTU domain-containing ubiquitin aldehyde binding 1 (OTUB1), leading to E2F1 deubiquitination and stabilization, thereby promotes BC malignant phenotypes. Furthermore, rescue experiments showed that TMPO-AS1 promotes BC growth in an E2F1-dependent manner.ConclusionsOur study is the first to uncover a novel positive regulatory loop of TMPO-AS1/E2F1 important for the promotion of BC malignant behaviors. The TMPO-AS1/E2F1 loop should be considered in the quest for new BC therapeutic options.

scholarly journals Inhibition of lncRNA TCONS_00077866 Ameliorates the High Stearic Acid Diet-Induced Mouse Pancreatic β-Cell Inflammatory Response by Increasing miR-297b-5p to Downregulate SAA3 Expression

2021 ◽  
Author(s):  
Huimin Lu ◽  
Rui Guo ◽  
Yunjin Zhang ◽  
Shenghan Su ◽  
Qingrui Zhao ◽  
...  
Keyword(s):  
Stearic Acid ◽  
Molecular Mechanisms ◽  
High Throughput Sequencing ◽  
Luciferase Reporter ◽  
Sequencing Analysis ◽  
Protective Effects ◽  
Β Cells ◽  
Β Cell ◽  
Shrna Expression ◽  
High Stearic Acid

Long-term consumption of a high-fat diet increases the circulating concentration of stearic acid (SA), which has a potent toxic effect on β-cells, but the underlying molecular mechanisms of this action have not been fully elucidated. Here, we evaluated the role of lncRNA TCONS_00077866 (lnc866) in SA-induced β<i>-</i>cell inflammation. lnc866 was selected for study because lncRNA high-throughput sequencing analysis demonstrated it to have the largest fold-difference in expression of five lncRNAs that were affected by SA treatment. Knockdown of lnc866 by virus-mediated shRNA expression in mice or by Smart Silencer in mouse pancreatic β-TC6 cells significantly inhibited the SA-induced reduction in insulin secretion and β-cell inflammation. According to lncRNA-microRNA (miRNAs)-mRNA co-expression network analysis and luciferase reporter assays, lnc866 directly bound to miR-297b-5p, thereby preventing it from reducing the expression of its target serum amyloid A3 (SAA3). Furthermore, overexpression of miR-297b-5p or inhibition of SAA3 also had marked protective effects against the deleterious effects of SA in β-TC6 cells and mouse islets. In conclusion, lnc866 silencing ameliorates SA-induced β<i>-</i>cell inflammation by targeting the miR-297b-5p/SAA3 axis. lnc866 inhibition may represent a new strategy to protect β-cells against the effects of SA during the development of type 2 diabetes.

scholarly journals Inhibition of lncRNA TCONS_00077866 Ameliorates the High Stearic Acid Diet-Induced Mouse Pancreatic β-Cell Inflammatory Response by Increasing miR-297b-5p to Downregulate SAA3 Expression

2021 ◽  
Author(s):  
Huimin Lu ◽  
Rui Guo ◽  
Yunjin Zhang ◽  
Shenghan Su ◽  
Qingrui Zhao ◽  
...  
Keyword(s):  
Stearic Acid ◽  
Molecular Mechanisms ◽  
High Throughput Sequencing ◽  
Luciferase Reporter ◽  
Sequencing Analysis ◽  
Protective Effects ◽  
Β Cells ◽  
Β Cell ◽  
Shrna Expression ◽  
High Stearic Acid

Long-term consumption of a high-fat diet increases the circulating concentration of stearic acid (SA), which has a potent toxic effect on β-cells, but the underlying molecular mechanisms of this action have not been fully elucidated. Here, we evaluated the role of lncRNA TCONS_00077866 (lnc866) in SA-induced β<i>-</i>cell inflammation. lnc866 was selected for study because lncRNA high-throughput sequencing analysis demonstrated it to have the largest fold-difference in expression of five lncRNAs that were affected by SA treatment. Knockdown of lnc866 by virus-mediated shRNA expression in mice or by Smart Silencer in mouse pancreatic β-TC6 cells significantly inhibited the SA-induced reduction in insulin secretion and β-cell inflammation. According to lncRNA-microRNA (miRNAs)-mRNA co-expression network analysis and luciferase reporter assays, lnc866 directly bound to miR-297b-5p, thereby preventing it from reducing the expression of its target serum amyloid A3 (SAA3). Furthermore, overexpression of miR-297b-5p or inhibition of SAA3 also had marked protective effects against the deleterious effects of SA in β-TC6 cells and mouse islets. In conclusion, lnc866 silencing ameliorates SA-induced β<i>-</i>cell inflammation by targeting the miR-297b-5p/SAA3 axis. lnc866 inhibition may represent a new strategy to protect β-cells against the effects of SA during the development of type 2 diabetes.

scholarly journals Inhibition of lncRNA TCONS_00077866 Ameliorates the High Stearic Acid Diet-Induced Mouse Pancreatic β-Cell Inflammatory Response by Increasing miR-297b-5p to Downregulate SAA3 Expression

2021 ◽  
Author(s):  
Huimin Lu ◽  
Rui Guo ◽  
Yunjin Zhang ◽  
Shenghan Su ◽  
Qingrui Zhao ◽  
...  
Keyword(s):  
Stearic Acid ◽  
Molecular Mechanisms ◽  
High Throughput Sequencing ◽  
Luciferase Reporter ◽  
Sequencing Analysis ◽  
Protective Effects ◽  
Β Cells ◽  
Β Cell ◽  
Shrna Expression ◽  
High Stearic Acid

Long-term consumption of a high-fat diet increases the circulating concentration of stearic acid (SA), which has a potent toxic effect on β-cells, but the underlying molecular mechanisms of this action have not been fully elucidated. Here, we evaluated the role of lncRNA TCONS_00077866 (lnc866) in SA-induced β<i>-</i>cell inflammation. lnc866 was selected for study because lncRNA high-throughput sequencing analysis demonstrated it to have the largest fold-difference in expression of five lncRNAs that were affected by SA treatment. Knockdown of lnc866 by virus-mediated shRNA expression in mice or by Smart Silencer in mouse pancreatic β-TC6 cells significantly inhibited the SA-induced reduction in insulin secretion and β-cell inflammation. According to lncRNA-microRNA (miRNAs)-mRNA co-expression network analysis and luciferase reporter assays, lnc866 directly bound to miR-297b-5p, thereby preventing it from reducing the expression of its target serum amyloid A3 (SAA3). Furthermore, overexpression of miR-297b-5p or inhibition of SAA3 also had marked protective effects against the deleterious effects of SA in β-TC6 cells and mouse islets. In conclusion, lnc866 silencing ameliorates SA-induced β<i>-</i>cell inflammation by targeting the miR-297b-5p/SAA3 axis. lnc866 inhibition may represent a new strategy to protect β-cells against the effects of SA during the development of type 2 diabetes.

scholarly journals Long Non-Coding RNA HAGLROS Promotes the Malignant Progression of Bladder Cancer by Regulating the miR-330-5p/SPRR1B Axis

2022 ◽  
Author(s):  
Shiwei Xiao ◽  
Yigang Zuo ◽  
Yanan Li ◽  
Yinglong Huang ◽  
Shi Fu ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Molecular Mechanisms ◽  
Subcellular Fractionation ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Sequencing Analysis ◽  
Loss Of Function ◽  
Invasion And Migration ◽  
Potential Biomarker ◽  
Underlying Mechanisms

Abstract BackgroundBladder cancer (BC) is the most common genitourinary malignancy worldwide, and its aetiology and pathogenesis remain unclear. Long noncoding RNAs can play vital roles in gene expression and diverse biological processes, especially in cancers. Accumulating evidence has shown that HAGLROS, a novel lncRNA, is closely related to the occurrence and progression of various cancers. However, the biological functions and underlying mechanisms of HAGLROS in BC remain unknown.MethodsThe relative expression of HAGLROS in BC was determined by bioinformatics analysis, transcriptome sequencing analysis and qRT–PCR. Gain- or loss-of-function assays were performed to study the biological roles of HAGLROS in BC. A CCK-8 assay was used to detect BC cell proliferation. BC cell invasion and migration were investigated by wound healing and Transwell assays. The cell cycle was analysed by flow cytometry assay. Western blot analysis and immunohistochemistry were performed to evaluate SPRR1B expression. The differential expression of candidate genes and their relationships were evaluated in data retrieved from the starBase database, the GEIPIA database, the Lnc2Cancer database and the LncBase database. FISH assays, subcellular fractionation assays and luciferase reporter assays were performed to explore the underlying molecular mechanisms of HAGLROS.ResultsHAGLROS expression is significantly upregulated in BC tissues and cells, and increasing HAGLROS expression was related to high pathologic grade. HAGLROS enhances the proliferation, migration and invasion of BC. Furthermore, SPRR1B is obviously upregulated and miR-330-5p is significantly downregulated in BC. Mechanistically, we found that HAGLROS is mainly located in the cytoplasm and positively regulates SPRR1B expression by sponging miR-330-5p, playing an oncogenic role in BC pathogenesis.ConclusionsThe present study demonstrates that HAGLROS is significantly overexpressed and plays an oncogenic role by regulating the miR-330-5p/SPRR1B axis in BC. HAGLROS may serve as a potential biomarker for the diagnosis and treatment of BC.

scholarly journals Induced GnasR201H expression from the endogenous Gnas locus causes fibrous dysplasia by up-regulating Wnt/β-catenin signaling

2017 ◽  
Vol 115 (3) ◽  
pp. E418-E427 ◽  
Author(s):  
Sanjoy Kumar Khan ◽  
Prem Swaroop Yadav ◽  
Gene Elliott ◽  
Dorothy Zhang Hu ◽  
Ruoshi Xu ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Fibrous Dysplasia ◽  
Molecular Mechanisms ◽  
Germ Line ◽  
Mendelian Inheritance ◽  
Bone Diseases ◽  
Cellular Mechanisms ◽  
Activating Mutations ◽  
Stimulatory G Protein

Fibrous dysplasia (FD; Online Mendelian Inheritance in Man no. 174800) is a crippling skeletal disease caused by activating mutations of the GNAS gene, which encodes the stimulatory G protein Gαs. FD can lead to severe adverse conditions such as bone deformity, fracture, and severe pain, leading to functional impairment and wheelchair confinement. So far there is no cure, as the underlying molecular and cellular mechanisms remain largely unknown and the lack of appropriate animal models has severely hampered FD research. Here we have investigated the cellular and molecular mechanisms underlying FD and tested its potential treatment by establishing a mouse model in which the human FD mutation (R201H) has been conditionally knocked into the corresponding mouse Gnas locus. We found that the germ-line FD mutant was embryonic lethal, and Cre-induced Gnas FD mutant expression in early osteochondral progenitors, osteoblast cells, or bone marrow stromal cells (BMSCs) recapitulated FD features. In addition, mosaic expression of FD mutant Gαs in BMSCs induced bone marrow fibrosis both cell autonomously and non-cell autonomously. Furthermore, Wnt/β-catenin signaling was up-regulated in FD mutant mouse bone and BMSCs undergoing osteogenic differentiation, as we have found in FD human tissue previously. Reduction of Wnt/β-catenin signaling by removing one Lrp6 copy in an FD mutant line significantly rescued the phenotypes. We demonstrate that induced expression of the FD Gαs mutant from the mouse endogenous Gnas locus exhibits human FD phenotypes in vivo, and that inhibitors of Wnt/β-catenin signaling may be repurposed for treating FD and other bone diseases caused by Gαs activation.

scholarly journals A Novel Identified Long Non-coding RNA, lncRNA MEF2C-AS1, Inhibits Cervical Cancer via Regulation of miR-592/RSPO1

2021 ◽  
Vol 8 ◽  
Author(s):  
Xiaoping Wang ◽  
Changhong Zhang ◽  
Meixuan Gong ◽  
Chen Jiang
Keyword(s):  
Cervical Cancer ◽  
Molecular Mechanisms ◽  
Survival Curve ◽  
The Cancer Genome Atlas ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Downstream Target ◽  
Qrt Pcr ◽  
Kaplan Meier ◽  
Downstream Target Gene

Purpose: Our purpose was to investigate the effect of lncRNA MEF2C antisense RNA 1 (MEF2C-AS1) on cervical cancer and further explore its underlying molecular mechanisms.Methods: The proliferation, migration and invasion of CC cells were determined by counting Kit-8 (CCK-8), colony formation assay, and transwell assays, respectively. qRT-PCR and western blot were conducted to quantitatively detect the expression of lncRNA MEF2C-AS1, miR-592 and R-spondin1 (RSPO1). Kaplan-Meier survival curve from the Cancer Genome Atlas (TCGA) database and the Gene Expression Profiling Interactive Analysis (GEPIA) website was used to describe the overall survival. Bioinformatics analysis was performed to search the downstream target of lncRNA MEF2C-AS1 and miR-592. Luciferase reporter assay was conducted to detect the interaction between lncRNA MEF2C-AS1 and miR-592 or miR-592 and RSPO1.Results: The data from GEPIA website showed that lncRNA MEF2C-AS1 expression was down-regulated in CC tissues and also associated with survival rate of CC patients. Moreover, the results of qRT-PCR also showed lncRNA MEF2C-AS1 was lowly expressed in CC cells. Subsequently, we confirmed that overexpression of lncRNA MEF2C-AS1 inhibited the proliferation, migration and invasion of CC cells. Further research illustrated that lncRNA MEF2C-AS1 was the target of miR-592, and RSPO1 was the downstream target gene of miR-592. Importantly, functional research findings indicated that lncRNA MEF2C-AS1 inhibited CC via suppressing miR-592 by targeting RSPO1.Conclusion: In our study, we demonstrated the functional role of the lncRNA MEF2C-AS1-miR-592-RSPO1 axis in the progression of CC, which provides a latent target for CC treatment.

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