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 IL-1β Pretreatment Improves the Efficacy of Mesenchymal Stem Cells on Acute Liver Failure by Enhancing CXCR4 Expression

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
He Nie ◽  
Fangmei An ◽  
Jie Mei ◽  
Cheng Yang ◽  
Qiang Zhan ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Inflammatory Diseases ◽  
Cxcr4 Expression ◽  
Migration Ability ◽  
Transwell Migration Assay ◽  
Migration Assay ◽  
Effective Therapeutic Strategy

Background. Mesenchymal stem cells (MSCs), with the powerful metabolic and functional supporting abilities for inflammatory diseases, may be an effective therapeutic strategy for acute liver failure (ALF). However, the efficacy of MSCs can still be promoted if pretreatment is applied to enhance their poor migration towards the damaged liver. The purpose of this study is to determine the effect of IL-1β pretreatment on the efficacy and homing ability of MSCs in ALF. Methods. MSCs were isolated by the whole bone marrow adherence method and characterized. The efficacy and homing ability of IL-1β-pretreated MSCs (Pre-MSCs) were examined in a rat ALF model and compared with that of MSCs and normal saline. Then, Western blot was performed to detect the c-Met and CXCR4 expression of MSCs and Pre-MSCs and followed by flow cytometry to detect the meaningful indicators. Finally, the migration abilities of different cells and different conditions were tested by the Transwell migration assay. Results. MSCs of ideal purity were successfully isolated and cultured. Comparing with MSCs, Pre-MSCs had significantly better efficacy on improving the survival rate and liver function of ALF rats. Further analyses of damaged liver tissues showed that IL-1β pretreatment significantly enhanced the efficacy of MSCs on suppressing liver necrosis. Besides, Pre-MSCs exhibited better effects in inhibiting apoptosis and activating proliferation. The results of tracing experiments with CM-Dil-labeled cells confirmed that more cells migrated to the damaged liver in the Pre-MSC group. In terms of mechanism, the CXCR4 expression was significantly enhanced by IL-1β pretreatment, and an increased migration ability towards SDF-1 that could be reversed by AMD3100 was found in Pre-MSCs. Conclusion. IL-1β pretreatment could enhance the homing ability of MSCs at least partially by increasing the expression of CXCR4 and further improve the efficacy of MSCs on ALF.

scholarly journals Lats1/2-Mediated Alteration of Hippo Signaling Pathway Regulates the Fate of Bone Marrow-Derived Mesenchymal Stem Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Lang Li ◽  
Liang Dong ◽  
Yifeng Wang ◽  
Xiuhong Zhang ◽  
Jie Yan
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Signaling Pathway ◽  
Vertical Migration ◽  
Transduction Efficiency ◽  
Hippo Signaling ◽  
Migration Assay ◽  
Hippo Signaling Pathway ◽  
Low Expression

Bone marrow-derived mesenchymal stem cells (BMSCs) can be used to enhance lung repair in acute respiratory distress syndrome (ARDS); however, the repairing effect is limited by poor homing and retention of BMSCs. The purpose of this study was to investigate whether Lats1 and Lats2-mediated alteration of Hippo signaling pathway could promote the differentiation, proliferation, and migration of BMSCs. BMSCs were transduced by lentiviral vectors for high and low expression of Lats1 and Lats2. The expression levels of Lats1, Lats2, YAP, and 14-3-3, respectively, were assessed to clarify the regulatory effects of Lats1 and Lats2 on Hippo signaling. Osteogenic (Runx2 and OSX) and adipogenic (C/EBPα and PPAR-γ) transcription factors were determined to clarify the effects of Hippo signaling on BMSCs differentiation. The effects of Hippo signaling on BMSCs proliferation and horizontal and vertical migration were also measured by CCK-8, scratch assay, and Transwell migration assay, respectively. Lentiviral transduction efficiency could reach 93.11%–97.14%. High and low expression of Lats1 and Lats2 could activate and inhibit the Hippo signaling pathway, respectively. High and low expression of Lats1 and Lats2 could inhibit and promote BMSCs differentiation into osteoblasts and adipocytes. High and low expression of Lats1 and Lats2 could inhibit and promote BMSCs proliferation and horizontal and vertical migration, respectively. Our studies suggest that Lats1/2-meidiated inhibition of Hippo signaling in BMSCs may optimize their effects of tissue repair in ARDS, suggesting a novel strategy for enhancing disease therapeutics.

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 Bone marrow mesenchymal stem cells derived from juvenile macaques reversed ovarian ageing in elderly macaques

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Chuan Tian ◽  
Jie He ◽  
Yuanyuan An ◽  
Zailing Yang ◽  
Donghai Yan ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Sex Hormones ◽  
Hormone Secretion ◽  
The Elderly ◽  
Differentially Expressed ◽  
Control Group ◽  
Functional Changes ◽  
Marrow Mesenchymal Stem Cells

Abstract Background Female sex hormone secretion and reproductive ability decrease with ageing. Bone marrow mesenchymal stem cells (BMMSCs) have been postulated to play a key role in treating ovarian ageing. Methods We used macaque ovarian ageing models to observe the structural and functional changes after juvenile BMMSC treatment. Moreover, RNA-seq was used to analyse the ovarian transcriptional expression profile and key pathways through which BMMSCs reverse ovarian ageing. Results In the elderly macaque models, the ovaries were atrophied, the regulation ability of sex hormones was reduced, the ovarian structure was destroyed, and only local atretic follicles were observed, in contrast with young rhesus monkeys. Intravenous infusion of BMMSCs in elderly macaques increased ovarian volume, strengthened the regulation ability of sex hormones, reduced the degree of pulmonary fibrosis, inhibited apoptosis, increased density of blood vessels, and promoted follicular regeneration. In addition, the ovarian expression characteristics of ageing-related genes of the elderly treatment group reverted to that of the young control group, 1258 genes that were differentially expressed, among which 415 genes upregulated with age were downregulated, 843 genes downregulated with age were upregulated after BMMSC treatment, and the top 20 differentially expressed genes (DEGs) in the protein-protein interaction (PPI) network were significantly enriched in oocyte meiosis and progesterone-mediated oocyte maturation pathways. Conclusion The BMMSCs derived from juvenile macaques can reverse ovarian ageing in elderly macaques.

scholarly journals Conditioned Medium of Bone Marrow Mesenchymal Stem Cells Relieves Acute Lung Injury in Mice by Regulating Epithelial Sodium Channels via miR-34c

2020 ◽  
Author(s):  
Zhiyu Zhou ◽  
Yong Cui ◽  
Yapeng Hou ◽  
Tong Yu ◽  
Yan Ding ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Conditioned Medium ◽  
Luciferase Reporter ◽  
Rt Pcr ◽  
Wide Range ◽  
Gene Assay

Abstract Aims: One of the characteristics of acute lung injury (ALI) is severe pulmonary edema, which is closelyrelated to alveolar fluid clearance. Mesenchymal stem cells (MSCs) secrete a wide range of cytokines,growth factors and miRNAs through paracrine action to participate in the mechanism of pulmonaryinflammatory response, which increases the clearance of edema fluid, and promotes the repair process ofALI. However, the mechanism by which bone marrow derived MSCs-conditioned medium (BMSCs-CM)promotes edema clearance is unclear. Epithelial sodium channel (ENaC) is the rate-limiting step in thesodium-water transport and edema clearance in the alveolar cavity, and we aim to explore the role of ENaCin BMSCs-CM invloved edema clearance and whether it can alter the function of ENaC via miRNAs.Methods: CCK-8 cell proliferation assay was used to detect the effect of BMSCs-CM on the survival ofAT2 cells. Real-time PCR (RT-PCR) and Western blot were used to detect the expression of ENaC in AT2cells. The effects of exosomes/miR-34c on the transepithelial short-circuit current in the monolayer of H441cells were examined by the Ussing chamber setup. Dual luciferase reporter gene assay was used to detect thetarget gene of miR-34c.Results: BMSCs-CM can increase the viability of mouse AT2 cells. RT-PCR and Western blotting resultsshowed that BMSCs-CM significantly increased the expression of γ-ENaC subunit in mouse AT2 cells.Ussing chamber assay revealed that BMSCs-CM enhanced the amiloride-sensitive currents associated withENaC activity in intact H441 cell monolayers. In addition, we observed higher expression of miR-34c inmouse AT2 cells administrated with BMSCs-CM, and the overexpression or inhibition of miR-34c canregulate the expression of ENaC protein and alter the function of ENaC. Finally, we detected MARCKS maybe one of the target gene of miR-34c.Conclusions: Our results indicate that BMSCs-CM may improve LPS-induced ALI through miR-34ctargeting MARCKS and regulating ENaC indirectly, which further explores the benefit of paracrine effectsof BMSCs on edematous ALI.

scholarly journals BMSC-Derived Exosomes Ameliorate Osteoarthritis by Inhibiting Pyroptosis of Cartilage via Delivering miR-326 Targeting HDAC3 and STAT1//NF-κB p65 to Chondrocytes

2021 ◽  
Vol 2021 ◽  
pp. 1-26
Author(s):  
Honggang Xu ◽  
Bin Xu
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Animal Experiments ◽  
Luciferase Reporter ◽  
Specific Gene ◽  
Migration Ability ◽  
Marrow Mesenchymal Stem Cells ◽  
Oa Chondrocytes ◽  
Related Proteins ◽  
And Cartilage

Background. In the past decade, mesenchymal stem cells (MSCs) have been widely used for the treatment of osteoarthritis (OA), and noncoding RNAs in exosomes may play a major role. Aim. The present study is aimed at exploring the effect and mechanism of miR-326 in exosomes secreted by bone marrow mesenchymal stem cells (BMSCs) on pyroptosis of cartilage and OA improvement. Methods. Exosomes from BMSCs (BMSC-Exos) were isolated and identified to incubate with OA chondrocytes. Proliferation, migration, specific gene and miR-326 expression, and pyroptosis of chondrocytes were detected. BMSCs or chondrocytes were transfected with miR-326 mimics or inhibitors to investigate the effect of miR-326 in BMSC-Exos on pyroptosis of chondrocytes and the potential mechanism. Finally, a rat OA model was established to verify the effect and mechanism of miR-326 in BMSC-Exos on cartilage of pyroptosis. Results. Incubation with BMSC-Exos could significantly improve the survival rate, migration ability, and chondrocyte-specific genes (COL2A1, SOX9, Agg, and Prg4) and miR-326 expression of OA chondrocytes and significantly inhibit pyroptosis of chondrocytes by downregulation of the levels of inflammatory cytokines, Caspase-1 activity, and pyroptosis-related proteins such as GSDMD, NLRP3, ASC, IL-1β, and IL-18 ( P < 0.01 ). PKH26 labeling confirmed the uptake of BMSC-Exos by chondrocytes. Incubation with exosomes extracted from BMSCs overexpressing miR-326 can significantly repress the pyroptosis of chondrocytes, while knockdown of miR-326 had the opposite effect ( P < 0.01 ). The same result was also demonstrated by direct interference with the expression level of miR-326 in chondrocytes ( P < 0.01 ). In addition, we found that the overexpression of miR-326 significantly inhibited the expression of HDAC3 and NF-κB p65 and significantly promoted the expression of STAT1, acetylated STAT1, and acetylated NF-κB p65 in chondrocytes ( P < 0.01 ). The targeted relationship between miR-326 and HDAC3 was verified by dual-luciferase reporter assay. Animal experiments confirmed the mechanism by which miR-326 delivered by BMSC-Exos inhibits pyroptosis of cartilage by targeting HDAC3 and STAT1/NF-κB p65 signaling pathway. Conclusion. BMSC-Exos can deliver miR-326 to chondrocytes and cartilage and improve OA by targeting HDAC3 and STAT1//NF-κB p65 to inhibit pyroptosis of chondrocytes and cartilage. Our findings provide a new mechanism for BMSC-Exos to treat OA.

scholarly journals Human amnion-derived mesenchymal stem cells promote osteogenic differentiation of lipopolysaccharide-induced human bone marrow mesenchymal stem cells via ANRIL/miR-125a/APC axis

2020 ◽  
Author(s):  
Yuli Wang ◽  
Fengyi Lv ◽  
Lintong Huang ◽  
Hengwei Zhang ◽  
Bing Li ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Osteogenic Differentiation ◽  
Noncoding Rna ◽  
Human Bone ◽  
Human Bone Marrow ◽  
Luciferase Reporter ◽  
Human Amnion ◽  
Marrow Mesenchymal Stem Cells

Abstract Background and aim: Periodontitis is a chronic inflammatory disease inducing the absorption of alveolar bone and leading to tooth loss. Human amnion–derived mesenchymal stem cells (HAMSCs) have been used for studying inflammatory processes. This study aimed to explore the role of long noncoding RNA (lncRNA) antisense noncoding RNA in the INK4 locus (ANRIL) in HAMSC-driven osteogenesis in lipopolysaccharide (LPS)-induced human bone marrow mesenchymal stem cells (HBMSCs).Methods: The cells were incubated with a co-culture system. Reactive oxygen species (ROS) level and superoxide dismutase (SOD) activity were used to detect the oxidative stress level. Flow cytometry was performed to determine cell proliferation. The alkaline phosphatase (ALP) activity, Alizarin red assay, cell transfection, and rat mandibular defect model were used to evaluate the osteogenic differentiation. Quantitative real-time reverse transcription–polymerase chain reaction (RT-PCR), Western blot analysis, dual-luciferase reporter assay, and immunofluorescence staining were used to evaluate the molecular mechanisms.Results: This study showed that HAMSCs promoted the osteogenesis of LPS-induced HBMSCs, while the ANRIL level in HBMSCs decreased during co-culture. ANRIL had no significant influence on the proliferation of LPS-induced HBMSCs. However, its overexpression inhibited the HAMSC-driven osteogenesis in vivo and in vitro, whereas its knockdown reversed these effects. Mechanistically, this study found that downregulating ANRIL led to the overexpression of microRNA-125a (miR-125a), and further contributed to the competitive binding of miR-125a and adenomatous polyposis coli (APC), thus significantly activating the Wnt/β-catenin pathway.Conclusion: The study indicated that HAMSCs promoted the osteogenic differentiation of LPS-induced HBMSCs via the ANRIL/miR-125a/APC axis, and offered a novel approach for periodontitis therapy.

Bone Marrow Mesenchymal Stem Cells (BMSCs)-Derived miR-31 in the Pathogenesis of Recurrent Abortion by Regulating Kisspeptins 1 (KISS1) Expression

2021 ◽  
Vol 11 (11) ◽  
pp. 2232-2238
Author(s):  
Ruiping Yu ◽  
Changfen Wu ◽  
Ying Qin ◽  
Cong Li ◽  
Zhongfu Mo ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Functional Recovery ◽  
Pregnancy Loss ◽  
Recurrent Pregnancy Loss ◽  
Fluorescent Protein ◽  
Endometrial Stromal Cells ◽  
Aberrant Expression ◽  
Marrow Mesenchymal Stem Cells

Bone marrow mesenchymal stem cells (BMSCs) are potentially efficacious in treating recurrent pregnancy disorders and endometrial injury. Uterine parenchymal cells interact with BMSCs to promote functional recovery. Our research aimed to explore the effect of BMSCs-derived miR-31 on recurrent pregnancy loss. A recurrent pregnancy loss mouse model was constructed followed by nanoparticle analysis of BMSC and miR-31 expressing by RT-PCR. The levels of miR-31 in BMSCs (miR-31+BMSCs or BMSCs) and their counterpart exosomes were up- or down-regulated to explore the effects of aberrant expression of miR-31 on endometrial damage in recurrent pregnancy loss. The analysis of BMSC nanoparticles showed that miR-31 was derived from BMSC. We found increased levels of miR-31 in miR-340 + BMSCs after incubation with endometrial stromal cells (ESCs) compared to controls. Labeling of exosomes by red fluorescent protein indicated that exosomes were liberated out of BMSCs and translocated into neighboring ESCs, and mice treated with miR-340 + BMSCs had improved functional recovery from recurrent pregnancy loss. BMSC-derived miR-31 mediates functional recovery induced in recurrent pregnancy miscarriage mice by regulating KISS1 expression and fibrosis gene expression.

MicroRNA-21 Derived from Exosomes of Bone Marrow Mesenchymal Stem Cells (BMSCs) Alleviates Pancreatic Cancer by Downregulation of a Disintegrin and Metalloprotease 9 (ADAM9)

2021 ◽  
Vol 11 (12) ◽  
pp. 2346-2356
Author(s):  
Jie Zhong ◽  
Juncheng Tang ◽  
Kun Huang
Keyword(s):  
Pancreatic Cancer ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Specific Inhibitor ◽  
Underlying Mechanism ◽  
Luciferase Reporter ◽  
Invasion And Migration ◽  
Marrow Mesenchymal Stem Cells ◽  
Novel Strategy

We aimed to explore underlying mechanism by which microRNA-21 (miR-21) derived from bone marrow mesenchymal stem cells (BMSCs) extracted exosomes (exo) in pancreatic cancer (PC). Bioinformatics analysis identified candidate miRNAs and target mRNAs in PC those were verified by luciferase reporter assay. BMSCs and exo were isolated and co-cultivated with PC cells. PC cells were then treated with plasmids loaded with miR-21 or a disintegrin and metalloprotease 9 (ADAM9), followed by detection of invasion, metastasis and apoptosis through Transwell assay and flow cytometry. MiR-21 was downregulated in PC tissues and cells, while ADAM9 was upregulated and positively correlated with poor prognosis. Overexpression of miR-21 restrained the capacities of proliferation, invasion and migration of PC cells by inhibiting ADAM9 expression. Specific inhibitor GW4869 reduced release of exo and declined miR-21 expression. Treatment with BMSC-exo containing miR-21 suppressed the malignant characteristics of cancer cells. MiR-21 derived from exo of BMSCs inhibited PC progression by ADAM9 down-regulation, providing insight into novel strategy against PC.

Bone Marrow Mesenchymal Stem Cells (BMSC)-Originated miR-133 Impedes Migration and Invasiveness of Glioma Cells While Enhancing Apoptosis via Targeting the Receptor for Activated C Kinase 1 (RACK1)

2021 ◽  
Vol 11 (9) ◽  
pp. 1818-1824
Author(s):  
Jiangbo Xiong ◽  
Sheng Liu ◽  
Bin Xiang ◽  
Weibo Zhang ◽  
Jun Du ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Glioma Cells ◽  
Luciferase Reporter ◽  
Mechanistic Study ◽  
Migration And Invasion ◽  
Luciferase Reporter Gene ◽  
Gene Assay ◽  
Marrow Mesenchymal Stem Cells

This study aims to dissect the effects of bone marrow mesenchymal stem cells (BMSC) on the in vitro activity of glioma cells and the underlying mechanisms. The glioma cells were transfected with miR-133 mimics, RACK1-Vector, negative control (NC) and miR-133 mimic+RACK1-Vector, respectively, and then co-cultured with BMSC followed by analysis of miR-133 expression via PCR, apoptosis via flow cytometry, proliferation via CCK-8, invasion and migration via Transwell assay, the expression of proteins involved in apoptosis, anti-apoptosis, invasiveness and RACK1 by western blot, and the targeting relationship between miR-133 and RACK1 by dual-luciferase reporter gene assay. In comparison with normal glial cells, glioma cells exhibited a significantly diminished miR-133 level. miR-133 was upregulated in glioma cells after co-culture with BMSC, along with significantly restrained proliferation rate, migration and invasion activities as well as reduced protein levels (MMP-2, Vimentin, N-cadherin and MMP-9). Mechanistic study showed that miR-133 can retard the expression of RACK1, thereby impeding the invasion, migration and proliferation activities of cells while triggering cell apoptosis. In conclusion, BMSC-originated miR-133 can impede the migration and invasion while enhancing the apoptosis of glioma cells via targeting RACK1.

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