Circ_0000274 contributes to renal cell carcinoma progression by regulating miR-338-3p/NUCB2 axis and JAK1/STAT3 pathway

BackgroundKidney transplant recipients (KTRs) are at increased risk of developing renal cell carcinoma (RCC). Accumulating evidence has demonstrated that circular RNAs (circRNAs) are essential players in tumor advancement. However, the functions of circ_0000274 in renal cell carcinoma (RCC) are barely explored.MethodsThe primary RCC cell lines 786-O and A498 were used in this study. Quantitative real-time polymerase chain reaction (qRT-PCR) assay was employed for the RNA levels of circ_0000274, microRNA-338-3p (miR-338-3p) and nucleobindin 2 (NUCB2). RNase R assay was conducted to analyze the feature of circ_0000274.Cell Counting Kit-8 (CCK-8) assay, colony formation assay, transwell assay, tube formation assay and flow cytometry analysis were conducted for cell viability, colony formation, metastasis, angiogenesis and apoptosis, respectively. Western blot assay was utilized for protein levels. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were adopted to analyze the associations of circ_0000274 RNA, miR-338-3p RNA and NUCB2 protein. Murine xenograft model was established to explore the function of circ_0000274 RNA in vivo. Immunohistochemistry (IHC) assay was used to analyze NUCB2 protein level in xenograft tumors.ResultsCompared to normal tissues and cells, circ_0000274 RNA level was elevated in RCC tissues and cells. Knockdown of circ_0000274 RNA suppressed cell viability, colony formation, metastasis and tube formation and promoted apoptosis in RCC cells in vitro. Circ_0000274 RNA sponged miR-338-3p RNA to positively regulate NUCB2 protein in RCC cells. Inhibition of miR-338-3p reversed the impacts of circ_0000274 knockdown on RCC cell malignant behaviors. MiR-338-3p RNA overexpression repressed the malignant phenotypes of RCC cells, while NUCB2 protein elevation could abrogate the effect. Moreover, circ_0000274 RNA knockdown blocked tumorigenesis in vivo. Besides, circ_0000274 RNA knockdown inactivated the JAK1/STAT3 protein signaling pathway.ConclusionCirc_0000274 RNA functioned as an oncogene in RCC development by regulating miR-338-3p RNA/NUCB2 protein axis and activating the JAK1/STAT3 protein signaling pathway.     

Circ_0008450 regulates keloid-derived fibroblast proliferation,migration, invasion and apoptosis with increased IGFBP5 through sponging miR-1224-5p

BackgroundKeloids (KD) are benign fibroproliferative tumors and circular RNAs (circRNAs) may participate in KD progression. At present, whether circ_0008450 regulates keloid-derived fibroblast phenotypes remains unclear. This study aimed to explore the functions of circ_0008450 in keloid (KD)-derived fibroblast phenotypes and the underlying mechanism.MethodsQuantitative real-time polymerase chain reaction (qRT-PCR) or western blot assay was performed to determine the expression of circ_0008450, miR-1224-5p, insulin like growth factor binding protein 5 (IGFBP5) and extracellular matrix (ECM)-related markers. 5-Ethynyl-2′-deoxyuridine (EdU) assay was conducted to assess cell proliferation ability. Flow cytometry analysis was used to analyze cell cycle and cell apoptosis. Scratch assay and transwell assay were utilized to examine cell migration and invasion. Mechanism assays were executed to verify the relations of circ_0008450, miR-1224-5p and IGFBP5.ResultsCirc_0008450 was highly expressed in KD tissues and KD-derived fibroblasts. Circ_0008450 silencing inhibited KD-derived fibroblast proliferation, cell cycle, and motility and promoted apoptosis. The effect of circ_0008450 knockdown on KD-derived fibroblast processes was ameliorated by miR-1224-5p downregulation. IGFBP5 was a target gene of miR-1224-5p. IGFBP5 upregulation abated miR-1224-5p-mediated effects on KD-derived fibroblast processes.ConclusionCirc_0008450 promoted KD-derived fibroblast proliferation, migration, and invasion and repressed apoptosis via sponging miR-1224-5p and elevating IGFBP5.     

Circular RNA circ_0114876 regulates osteoarthritis through upregulating ADAM10 via targeting miR-1227-3p

BackgroundOsteoarthritis (OA) was a chronic degenerative joint disease. The dysregulation of circular RNAs (circRNAs) has been identified in OA progression. However, the function and regulation mechanism of circ_0114876 in OA remains largely unknown.MethodFirstly, we used LPS-treated C28/I2 cells as a cellular model of OA. Quantificational real-time polymerase chain reaction (qRT-PCR) was used to determine the expression levels of circ_0114876, miRNA-1227-3p, and ADAM10 in OA chondrocytes. Cell Counting Kit-8 (CCK8), 5-ethynyl-20-deoxyuridine (EdU) incorporation assays, flow cytometry, Enzyme-linked immunosorbent assay (ELISA) kit, and western blot were applied to confirm cell proliferation, apoptosis, inflammation, and extracellular matrix.of circ_0114876 in vitro. The interaction between circ_0114876 and its downstream target (miR-1227-3p) and mRNA target ADAM metallopeptidase domain 10 (ADAM10), was evaluated by luciferase assay and RNA immunoprecipitation (RIP) assay.ResultCirc_0114876 and ADAM10 were upregulated and miR-1227-3p was decreased in OA tissues and LPS-treated chondrocytes. Low expression of circ_0114876 promoted proliferation and inhibited apoptosis, inflammation, and extracellular matrix of the LPS-treated chondrocytes. Mechanistically, circ_0114876 functioned in human chondrocytes through targeting miR-1227-3p and ADAM10. Furthermore, miRNA-1227-3p inhibitor reversed the effect of circ_0114876 knockdown on the OA chondrocytes, and ADAM10 overexpression reversed the effect of miR-1227-3p mimic on the OA chondrocytes.ConclusionCirc_0114876 was increased in OA tissues and cells. Circ_0114876 facilitated the progression in the LPS-induced OA cell model via regulating the miR-1227-3p/ADAM10 axis. This study would provide a potentially effective therapeutic strategy for OA progression.     

Knockdown of circ_0026579 ameliorates lipopolysaccharide (bacterial origin)-induced inflammatory injury in bronchial epithelium cells by targeting miR-338-3p/TBL1XR1 axis

BackgroundCircular RNAs (circRNAs) play an important regulatory role in human diseases including organ allograft rejection. The aim of this study is to clarify the functional role and molecular mechanism of circ_0026579 RNA in lipopolysaccharide (LPS)-induced bronchopneumonia injury.Materials and methodsBronchial epithelial BEAS-2B cells were treated with LPS to mimic an in vitro model for bronchopneumonia. Cell viability and proliferation were analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and 5-ethynyl-2′-deoxyuridine (EdU) assay. Flow cytometry assay was used to assess cell apoptosis. Caspase-3 activity was analyzed by Caspase-3 activity assay kit. The expression levels of circ_0026579 RNA, miR-338-3p, and transducin β-like 1× related protein 1 (TBL1XR1) RNA were determined by RT-qPCR. The protein level was quantified by western blot assay. The correlation between miR-338-3p and circ_0026579 or TBL1XR1 was confirmed by dual-luciferase reporter and RNA immunoprecipitation assays.ResultsLPS treatment repressed proliferation but induced apoptosis and inflammatory response in BEAS-2B cells. Circ_0026579 RNA was highly expressed in patients with pneumonia. Besides, the expression levels of circ_0026579 RNA and TBL1XR1 RNA/protein were upregulated, while miR-338-3p level was decreased in LPS-treated BEAS-2B cells. Knockdown of circ_0026579 RNA or TBL1XR1 protein could abolish LPS-induced cell injury in BEAS-2B cells. Furthermore, we found that circ_0026579 RNA functioned as a “sponge” for miR-338-3p to regulate TBL1XR1 expression. Additionally, silencing circ_0026579 RNA protected BEAS-2B cells from LPS-induced bronchopneumonia injury by regulating TBL1XR1 expression.ConclusionCirc_0026579 RNA knockdown promoted cell proliferation but inhibited apoptosis and inflammation in LPS-induced BEAS-2B cells through regulating miR-338-3p RNA/TBL1XR1 protein axis.     

Depletion of circ_0006459 protects human brain microvascular endothelial cells from oxygen-glucose deprivation-induced damage through the miR-940/FOXJ2 pathway

BackgroundMultiple circular RNAs (circRNAs) play important roles in ischemic stroke. The present study aims to reveal the role and the mechanism of circ_0006459 in ischemic stroke.MethodsHuman brain microvascular endothelial cells (HBMECs) were treated with oxygen-glucose deprivation (OGD) to mimic an in vitro ischemic stroke model. RNA expression of circ_0006459, microRNA-940 (miR-940), and forkhead box J2 (FOXJ2) was detected by quantitative real-time polymerase chain reaction. Cell proliferation was analyzed by cell counting kit-8 (CCK-8) and 5-Ethynyl-29-deoxyuridine (EdU) assays. Cell apoptotic rate was quantified by flow cytometry analysis. The protein expression of proliferating cell nuclear antigen (PCNA), clusters of differentiation 6 (CDK6), BCL2-associated x protein (Bax), B-cell lymphoma 2 (Bcl2), interleukin-1β (IL-1β), IL-8, IL-18 and tumor necrosis factor-α (TNF-α) was analyzed by Western blotting. The regulatory relationships among circ_0006459, miR-940, and F 《人生只有一件事》 OXJ2 were identified by dual-luciferase reporter assay, RNA immunoprecipitation assay, and RNA pull-down assay.ResultsCirc_0006459 and FOXJ2 expression were significantly upregulated, whereas miR-940 expression was downregulated in HBMECs after OGD. Circ_0006459 depletion assuaged OGD-induced inhibition in cell proliferation and promotion in cell apoptosis and inflammation in HBMECs. Circ_0006459 acted as a sponge for miR-940, and miR-940 targeted FOXJ2 in HBMECs. Besides, miR-940 silencing or FOXJ2 overexpression relieved circ_0006459 knockdown-induced promotion in cell proliferation and inhibition in cell apoptosis and inflammation in OGD-induced HBMECs. Further, circ_0006459 depletion decreased FOXJ2 protein expression by interacting with miR-940.ConclusionDepletion of circ_0006459 protected human brain microvascular endothelial cells from oxygen-glucose deprivation-induced damage through miR-940/FOXJ2 pathway, providing a promising therapeutic target for ischemic stroke.     

Circ_0061140 stimulates the malignant development of prostate cancer by targeting miR-1193

BackgroundThis study sought to explore the expression pattern in prostate cancer (PCa) tissues, as well as the regulatory effects of circ_0061140 on the proliferative potential of PCa cells.MethodsA quantitative real-time polymerase chain reaction (qRT-PCR) analysis was undertaken to detect circ_0061140 levels in 43 paired PCa tissues and adjacent normal tissues. After the knockdown of circ_0061140, changes in the proliferative potential of PCa cells and tumor growth in nude mice with PCa were detected. Finally, the relationship of circ_0061140 and miR-1193 in the development of PCa was assessed.ResultsThe results showed that circ_0061140 was upregulated in PCa tissues. PCa patients with higher Gleason score or larger sized tumors expressed higher levels of circ_0061140. Additionally, the knockdown of circ_0061140 inhibited the proliferative potential of PCa cells. MiR-1193 was the target gene binding circ_0061140, and its level was negatively regulated by circ_0061140. Finally, rescue experiments showed that miR-1193 was regulated by circ_0061140 in the development of PCa.ConclusionsCirc_0061140 is upregulated in PCa tissues, and is closely linked to Gleason score and tumor size in PCa. Additionally, it causes PCa cells to proliferate by negatively regulating miR-1193.     

miR-195-5p通过靶向ROCK1抑制肾癌细胞迁移、侵袭和上皮-间质转化

目的探讨miR-195-5p对肾癌细胞迁移、侵袭和上皮-间质转化的影响。方法通过转染miR-195-5p mimics或inhibitors分别过表达或抑制肾癌细胞中miR-195-5p的表达,转染靶向Rho相关螺旋蛋白激酶1(ROCK1)的小干扰RNA敲低肾癌细胞中ROCK1的表达量,利用细胞划痕实验和Transwell小室实验分别检测肾癌细胞的迁移和侵袭能力。通过双荧光素酶报告实验验证miR-195-5p对ROCK1的靶向调控作用,利用免疫印迹试验检测ROCK1及上皮-间质转化相关蛋白的表达水平。结果过表达miR-195-5p可显著抑制肾癌细胞的迁移、侵袭和上皮-间质转化,而抑制miR-195-5p的表达可明显促进肾癌细胞的迁移、侵袭和上皮-间质转化(P<0.05)。miR-195-5p可通过靶向ROCK1调控其在肾癌细胞中表达。敲低ROCK1后可部分抵消miR-195-5p inhibitors对肾癌细胞迁移、侵袭和上皮-间质转化的影响。结论miR-195-5p可通过靶向ROCK1抑制肾癌细胞的迁移、侵袭和上皮-间质转化。     

MicroRNA-199a-3p在肾癌中的表达及作用

目的 检测microRNA-199a-3p(miR-199a-3p)在肾癌细胞株和组织中的表达情况并探究miR-199a-3p在肾癌细胞中的作用.方法 利用实时定量RT-PCR检测miR-199a-3p在肾癌细胞和组织中的表达水平;利用miR-199a-3p模拟物转染肾癌细胞786-0上调miR-199a-3p后,通过CCK-8、克隆形成、Transwell以及细胞周期检测来探究其在肾癌细胞中的作用.结果 miR-199a-3p在肾癌细胞中明显低表达,在78%(14/18)的肾癌组织中亦明显低表达;上调miR-199a-3p可显著抑制肾癌细胞的增殖、存活和侵袭并能诱导细胞周期G1期阻滞.结论 我们的研究显示在肾癌中miR-199a-3p明显低表达并参与肾癌的发生、发展,这表明miR-199a-3p具有作为肾癌诊断和治疗靶点的潜能.     

Hsa_circ_0010729 regulates H2O2-induced myocardial injury by regulating miR-1184/RIPK1 axis

BackgroundIschemia-reperfusion (I/R) is an important risk factor for cardiovascular diseases (CVDs) and cardiac transplantation, as I/R can cause myocardial cell hypoxia/reoxygenation (H/R) injury. Recent research has shown that circular RNAs (circRNAs) may affect the progress of H/R-induced myocardial injury, but the mechanism remains unknown. Our work explored the role of circ_0010729 in H2O2-induced myocardial injury.MethodsThe levels of circ_0010729, microRNA-1184 (miR-1184) and mRNA of receptor interacting serine/threonine kinase 1 (RIPK1) were indicated by quantitative real-time polymerase chain reaction (qRT-PCR) in human cardiac myocytes (HCMs). Meanwhile, the protein level of RIPK1 was quantified by western blot analysis. Besides, the cell functions were examined by 5-Ethynyl-29-deoxyuridine (EdU) assay, flow cytometry assay, western blot and antioxidant indexes analysis. Furthermore, the interplay between miR-1184 and circ_0010729 or RIPK1 was detected by dual-luciferase reporter assay. Eventually, the in vivo experiments were applied to measure the role of circ_0010729.ResultsThe levels of circ_0010729 RNA and RIPK1 protein were increased, and the miR-1184 was decreased in HCMs exposed to H₂O₂. In functional analysis, circ_0010729 deficiency restrained cell apoptosis and oxidative stress, whereas promoted cell proliferation in HCMs under H₂O₂ exposure. Moreover, miR-1184 inhibited the H₂O₂-induced myocardial injury by targeting RIPK1. Mechanistically, circ_0010729 acted as a miR-1184 sponge to regulate the level of RIPK1.ConclusionCirc_0010729 promotes H₂O₂-induced myocardial injury, and thus circ_001729 may be targeted as a potential therapy for H/R-induced myocardial injury.     

miR-181a-5p通过HOXB4抑制骨肉瘤细胞HOS增殖和迁移

目的：研究miR-181a-5p对HOS骨肉瘤细胞增殖、周期和迁移的影响及其机制。方法 ：采用实时定量PCR检测hFOB1.19成骨细胞和HOS、U2OS、MG63骨肉瘤细胞系中miR-181a-5p及HOXB4的表达情况。利用Lipofectamine 2000将miR-181a-5p mimics和miR-181a-5p inhibitor分别转染至人骨肉瘤HOS细胞中（分别为过表达组和抑制剂组）,并设置miR阴性对照组;CCK-8法检测各组细胞的增殖能力变化,流式细胞术检测各组细胞的细胞周期变化,划痕愈合实验以及Transwell迁移实验检测各组细胞的迁移能力变化。Targetscan网站预测miR-181a-5p的靶向基因,并通过双荧光素酶报告基因系统及Western blot验证靶向关系。结果：与成骨细胞hFOB1.19相比,miR-181a-5p在骨肉瘤细胞HOS、U2OS和MG63中低表达（P<0.05）,而HOXB4在骨肉瘤中高表达（P<0.05）。与阴性对照组相比,过表达miR-181a-5p抑制骨肉瘤HOS细胞的增殖和迁移能力,并且处于细胞周期S期的细胞...     

MicroRNA-106a-5p alleviated the resistance of cisplatin in lung cancer cells by targeting Jumonji domain containing 6

BackgroundCisplatin (DDP) is used for lung cancer therapy. MicroRNAs, small non-coding RNAs, may contribute to tumorigenesis as well as to drug resistance. We examined regulatory functions of miR-106a-5p in DDP-resistant lung cancer cells.MethodsDifferentially expressed miRNAs were provided by Gene Expression Omnibus (GEO) datasets and RT-qPCR examined RNA levels of miR-106a-5p and Jumonji domain-containing protein 6 (JMJD6), an enzyme causing lysine hydroxylation and arginine demethylation. Bindings were determined by luciferase reporter assay. Additionally, the half maximal inhibitory concentration (IC₅₀) of DDP was determined through Cell Counting Kit-8 (CCK-8) after treated by DDP (0, 6.25, 12.5, 25, 50 and 75 μM) and apoptosis rates were analyzed using flow cytometry. Besides that, migratory ability and invasiveness were examined by transwell. Western blot was for measuring protein levels of Bcl-2, Bax in apoptosis and E-cadherin, N-cadherin in epithelial-mesenchymal transition (EMT).ResultsThe IC₅₀ value of DDP-resistant A549 (A549/DDP) cells was higher, so were migration, invasion and N-cadherin in EMT while the apoptosis and E-cadherin in EMT were lower versus the parental A549 cells (no DDP resistance). MiR-106a-5p was low expressed in A549/DDP cells while its overexpression caused decreased migration, invasiveness and EMT but promoted apoptosis. JMJD6 was directly targeted and negatively regulated by miR-106a-5p. Inhibited JMJD6 decreased migratory ability, invasion and EMT but improved apoptosis. Moreover, knockdown of miR-106a-5p induced high level of JMJD6, migration, invasiveness and EMT but low apoptosis rates, which were restrained by JMJD6 suppression.ConclusionMiR-106a-5p/JMJD6 axis accelerated cell apoptosis and suppressed invasiveness, migration and EMT in A549/DDP cells.     

微小RNA-23a-5p/肿瘤蛋白53诱导的核蛋白1调控胰腺癌细胞吉西他滨耐药的实验研究

目的:探讨微小RNA(microRNA,miR)调控胰腺癌吉西他滨耐药的分子作用机制。方法:反转录聚合酶链反应(qPCR)检测来自桂林医学院附属医院2015年1月至2018年12月收治的胰腺癌患者的临床标本miR-23a-5p表达水平,细胞实验检测miR-23a-5p对吉西他滨处理下肿瘤蛋白53诱导的核蛋白1(TP53...     

CircSLC8A1 targets miR-181a-5p/HIF1AN pathway to inhibit the growth,migration and extracellular matrix deposition of human keloid fibroblasts

BackgroundCircular RNAs (circRNAs) are identified as important regulators in human diseases, including keloid. The purpose of this study is to reveal the role and molecular mechanism of circSLC8A1 in keloid formation.MethodsExpression of circSLC8A1, microRNA (miR)-181a-5p, and hypoxia inducible factor 1 alpha inhibitor (HIF1AN) were detected by quantitative real-time PCR. Protein expression of extracellular matrix (ECM) deposition markers and HIF1AN was detected by western blot analysis. Furthermore, the interaction between miR-181a-5p and circSLC8A1 or HIF1AN was confirmed by dual-luciferase reporter assay, RIP assay and RNA pull-down assay.ResultsExpression of circSLC8A1 was downregulated in keloid tissues and HKFs. Overexpression of circSLC8A1 suppressed HKFs proliferation, migration, ECM deposition, and promoted apoptosis. MiR-181a-5p is targeted by circSLC8A1, and its mimic reversed the effect of circSLC8A1 on the biological function of HKFs. HIF1AN was a target of miR-181a-5p, and it was positively regulated by circSLC8A1. Knockdown of HIF1AN also reversed the negatively regulation of circSLC8A1 on the biological functions of HKFs.ConclusionOur data showed that circSLC8A1 regulates the miR-181a-5p/HIF1AN axis to restrain HKFs biological functions, confirming that circSLC8A1 might serve as a novel therapeutic target for keloids.     

Exosomal circ_HIPK3 reduces apoptosis in H2O2-induced AC16 cardiomyocytes through miR-33a-5p/IRS1 axis

BackgroundExosomal circular RNAs (circRNAs) has been revealed to participate in the processes of cellular angiogenesis, growth and metastasis. Herein, the goal of this work was to investigate the role of exosomal circ_HIPK3 in cardiomyocyte apoptosis.MethodsExosomes were isolated using ultracentrifugation method and observed by transmission electron microscopy (TEM). Western blot was used to detect exosomes markers. The experimental group AC16 cells were exposed to hydrogen peroxide (H2O2). Levels of genes and proteins was detected by qRT-PCR and Western blot. EdU assay, CCK8 assay, flow cytometry, and Western blot were utilized to detect the function of exosomal circ_HIPK3 in proliferation, and apoptosis. The target relationship between miR-33a-5p and circ_HIPK3 or IRS1 (insulin receptor substrate 1).ResultsCirc_HIPK3 was packaged into exosomes and derived from AC16 cells. The expression of circ_HIPK3 was decreased by H2O2 treatment in AC16 cells, which also led to the decrease of circ_HIPK3 in exosomes. Functional analysis showed exosomal circ_HIPK3 promoted AC16 cell proliferation and reduced cell apoptosis under H2O2 treatment. Mechanistically, circ_HIPK3 acted as a sponge of miR-33a-5p to up-regulate the expression of its target IRS1. Functionally, forced expression of miR-33a-5p reversed the reduction of exosomal circ_HIPK3 in apoptosis of H2O2-stimulated AC16 cells. Moreover, miR-33a-5p inhibition contributed to the proliferation of H2O2-stimulated AC16 cells, which was abolished by IRS1 silencing.ConclusionExosomal circ_HIPK3 reduced H2O2-induced AC16 cardiomyocyte apoptosis through miR-33a-5p/IRS1 axis, suggesting a novel insight into the pathology of myocardial infarction.     

反义miR-30a-5p对人脑胶质瘤细胞U251生长的抑制作用

目的 观察敲低microRNA(miR)-30a-5p表达对人脑胶质瘤U251细胞生物学特征的影响.方法 用脂质体介导转染寡聚核苷酸抑制物(miR-30a-5p inhibitor)于人脑胶质瘤U251细胞.采用实时聚合酶链反应(real-time PCR)检测转染后U251细胞的miR-30a-5p表达水平以鉴定抑制效果;噻唑蓝(MTT)比色法评价miR-30a-5p inhibitor抑制U251细胞生长的作用;Transwell实验检测细胞侵袭能力变化;流式细胞术检测细胞周期变化;Annexin V法检测细胞早期凋亡.结果 real-time PCR检测结果 显示转染miR-30a-5p inhibitor后,肿瘤细胞miR-30a-5p表达下降,细胞增殖活性降低,细胞侵袭能力明显受到抑制,细胞周期阻滞在G0/G1期及早期凋亡增加.结论 miR-30a-5p可能是癌微RNA(oncomiR)之一,有望成为人脑胶质瘤基因治疗的候选靶点.

Abstract：

Objective To investigate the effect of knock-down of miR-30a-5p on the biological characteristics of U251 glioblastoma cells. Methods miR-30a-5p inhibitor, mediated by Lipofectamine 2000, was transfected to U251 cells for knocking down miR-30a-5p. Real-time polymerase chain reaction (PCR) was conducted to detect the expression of miR-30a-5p in transfected cells. The cell proliferation rate was detected by methyl thiazol tetrazolium (MTT) assay, and cell cycle kinetics was examined by flow cytometry. The cell invasive ability was evaluated by Transwell assay and apoptosis detected by Annexin V assay. Results The expression of miR-30a-5p in the miR-30a-5p inhibitor group was significantly down-regulated. The cell proliferation activity and invasive ability were reduced. Cells were arrested in G0/G1 phase, and apoptosis was induced in cells transfected with miR-30a-5p inhibitor as compared to those of the cells transfected with scramble siRNA and control cells, so suppression of miR-30a-5p expression rendered the glioma cells harboring less aggressive phenotype. Conclusion miR-30a-5p is one of oncomiRs. It may be a candidate target miRNA for gene therapy of gliomas.