Synergistic Effects of Taurine and Temozolomide Via Cell Proliferation Inhibition and Apoptotic Induction on U-251 MG Human Glioblastoma Cells

Objective: The combination treatment is a way to improve the therapeutic strategy of temozolomide (TMZ) -resistant glioblastoma (GBM). Taurine (TAU) has the potential to inhibit growth in various cancer cells. The aim of this study was to examine the combined effects of TMZ and TAU on cultured human GBM, U-251 MG cells. Methods: The cells were incubated with TMZ, TAU, and the combination of both in various ratios. MTT assay was performed to measure the cell viability of the treatments and then the synergistic interactions were evaluated by the Chou-Talalay method. The cell cycle and apoptotic properties of the combined treatment on U-251 MG cells were examined by flow cytometry. The Hoechst 33342 stainings were applied to visualize the morphologic change in the apoptotic process. Results: The combined treatment with a dose reduction of each expressed synergistic effect on the decrease of cell viability. The study on the cell cycle resulted in G2/M phase arrest with increasing apoptotic cells in the SubG1 phase. Moreover, the apoptotic effects of the combinations on U-251 MG cells were explained by the increase of apoptotic cells in both early and late stages and illustrated by some characteristics of the apoptotic process including condensed chromatin and fragmented nuclei. Conclusion: The study showed that the combination between TMZ and TAU has a potential in anticancer properties against U-251 MG manifested by the induction of G2/M arrest and apoptosis. These results suggest that this combination may be useful to enhance the efficacy and reduce some adverse events of GBM treatment in the future.     

Potential Mechanisms of Benzyl Isothiocyanate Suppression of Invasion and Angiogenesis by the U87MG Human Glioma Cell Line

Glioma is one of the most common tumors in China and chemotherapy is critical for its treatment. Recentstudies showed that benzyl isothiocyanate (BITC) could inhibit the growth of glioma cells, but the mechanisms arenot fully understood. This study explored the inhibitory effect of BITC on invasion and angiogenesis of U87MGhuman glioma cells in vitro and in vivo, as well as potential mechanisms. It was found that BITC could inhibitinvasion and angiogenesis of human glioma U87MG cells by inducing cell cycle arrest at phase G2/M. It alsowas demonstrated that BITC decreased expression of cyclin B1, p21, MMP-2/9, VE-cadherin, CD44, CXCR4and MTH1, the activity of the telomerase and PKCζ pathway. Microarray analysis was thus useful to explorethe potential target genes related to tumorigenic processes. BITC may play important roles in the inhibition ofinvasion and angiogenesis of human glioma cells.     

Drug-induced Apoptosis by Anti-microtubule Agent,Estramustine Phosphate on Human Malignant Glioma Cell Line,U87MG; in vitro Study

The drug effect of estramustine phosphate (EMP), an anti-microtubule agent on human glioma cells has been studied with the focus being mainly its cytotoxity or its targeting of organelles. However, the pharmacological knowledge of estramustine with respect to its cytotoxity and mechanism is limited. To acquire such knowledge, the present study investigates the ability of EMP to induce apoptosis in a human malignant glioma cell line. Transmission electron microscope (TEM) images were examined to monitor periodic changes. Agarose gel electrophoresis was also examined. Cellular DNA fragmentation ELISA was performed to investigate the DNA fragmentation rates and an MTT assay was studied to evaluate the ID₅₀. A TEM study revealed condensing and fragmentation of the chromatin. Laddering of the bands was observed in all EMP exposure groups in agarose gel electrophoresis. DNA fragmentation in all EMP groups began at 0.5h following an exposure with EMP and increased in a dose- and time-dependent manner as revealed by DNA ELISA fragmentation. ID₅₀ at 24h was 5.0µM according to the MTT assay, a value close to 4.8µM of ID₅₀ was revealed by the DNA fragmentation assay. None of the above mentioned changes was observed in the control group. These results indicated that EMP caused a drug-induced apoptosis in the human malignant glioma cell line, U87MG.     

Promising Fusion Protein Design to Target the U87 MG Glioma Cell Line

Gliomas, with a poor clinical course, account for 30% to 40% of all intracranial tumors. Immunotherapywith monoclonal antibodies has emerged as a promising area of investigation and recently it has been shown thatantibodies utilize complementarity-determining regions (CDRs) of their variable domains to bind to antigenswith high affinity and specificity. Here, we designed an antibody mimetic fused with diphtheria toxin to targetthe U87 MG glioma cell line. VHCDR1 and VLCDR3, together with 5 amino acid residues on both side of theCDRs, through a cognate framework region (VHFR2) yielded a mimetic of BT32/A6 (United States Patentnumber: 5639863). We fused the mimetic with the first 388 amino acid residues of diphtheria toxin and E. colistrain BL21 (ED3) was used to express the soluble immunotoxin DT-MG. The immunotoxin DT-MG alone didnot kill Raji up to the maximal concentration tested (10-6M) in vitro. By contrast, concentrations ≥10-9M, of thefused DT-MG killed more than 95% of U-87 MG cells. It is suggested that the mimetic maintained the synergicinteractions and high-affinity associated with the parent antibody. This construct holds promise for targetingspecific cancer epitopes and may be useful when incorporated into diagnostic and therapeutic regimens.     

Increasing of HER2 Membranar Density in Human Glioblastoma U251MG Cell Line Established in a New Nude Mice Model

Glioblastoma multiform (GBM) remains the most devastating primary tumour in neuro-oncology. Human Epithelial Receptor Type 2 (HER2) is a transmembrane tyrosine/kinase receptor that is important for cancer growth. HER2 is not expressed in adult glial cells, but its expression increases with the degree of astrocytomas anaplasia. We have recently demonstrated the ability of anti-HER2 antibodies to induce in vitro apoptosis GBM cell lines; this ability is correlated to HER2 density. A decreasing of tyrosine/kinase receptors density during in vitro culture was reported. No information exists about the variation of HER2 expression after in vivo implantation. For that, the two cell lines in vitro tested (U251MG, A172) were in vivo implanted. We established a U251MG in vivo model in balb/c nude mice showing an important increasing of HER2 density. The HER2 density is correlated to anti-HER2 antibody efficiency so this model will be useful for the evaluation of in vivo anti-HER2 antibody treatment.     

二氯乙酸钠对人骨肉瘤MG63细胞周期及凋亡影响的初步研究

目的 探讨不同浓度的二氯乙酸钠(DCA)对人骨肉瘤MG63细胞活性、周期及凋亡的影响.方法 用含质量分数10％胎牛血清的RPMI-1640培养基培养MG63细胞,不同浓度DCA作用于对数生长期的细胞,CCK8试剂盒检测50、100、200 μg·mL-1DCA处理24 h、48 h后细胞增殖情况;流式细胞术检测100、200 μg·mL-1 DCA-Na作用24 h、48 h后细胞周期和凋亡情况;qRT-PCR检测100、200 μg·mL-1DCA处理后细胞周期相关基因CDK2的变化.结果 CCK8检测结果显示50、100、200 μg· mL-1DCA均能抑制MG63细胞的生长,且有时间和浓度依赖性;不同浓度的DCA-Na分别干预MG63细胞不同时间后都明显阻滞细胞于G2/M期,且细胞凋亡率增加(P均＜0.001);不同浓度的DCA干预MG63细胞后,细胞中的CDK2mRNA的相对表达量明显降低(P均＜0.001).结论 DCA通过抑制CDK2使MG63细胞阻滞于G2/M期,进而诱导细胞凋亡,抑制细胞的生长.     

反义封闭MMP-9基因表达对胶质母细胞瘤细胞系增殖的影响

目的 探讨反义封闭胶质瘤细胞MMP-9基因表达对胶质瘤细胞增殖的影响。方法 利用基因重组的方法构建正义和反义MMP-9重组体;经脂质体介导,分别将pcDNA3.0空载质粒、正义重组体、反义重组体转染TJ905细胞;通过RT-PCR和Western blot检测转染细胞MMP-9的mRNA和蛋白表达水平;利用免疫组织化学法分析了转染细胞中MMP-9和Ki-67的表达。结果经限制性酶切鉴定和DNA测序分析,基因重组成功,且正义与反义重组体插入位点间的序列方向正好相反。与TJ905对照组、空载体组和正义对照组相比较,转染反义重组体后的TJ905细胞中MMP-9 mRNA和蛋白的表达水平明显下降（P<0.001）。转染空载体和正义重组体后,TJ905细胞内MMP-9 mRNA和蛋白的表达水平与未进行转染的TJ905细胞相比差异无统计学差异（P>0.05）。免疫组织化学结果显示反义封闭有效,MMP-9的表达下调,TJ905细胞增殖活性下降。结论 转染反义MMP-9重组体可以有效抑制胶质母细胞瘤细胞的MMP-9基因的表达,同时可以抑制肿瘤细胞的增殖。     

Constitutive Activation of the Neuregulin-1/erbB Signaling Pathway Promotes the Proliferation of a Human Peripheral Neuroepithelioma Cell Line

Neuregulin-1 (NRG-1) proteins, acting through their erbB receptors, promote the differentiation, survival and/or proliferation of many cell types in the developing nervous system, including neural crest cells and neural crest-derived Schwann cells. We have recently found that the proliferation of a neoplastic Schwann cell line is dependent on constitutive activation of the NRG-1/erbB signaling pathway and that overexpression of NRG-1 in myelinating Schwann cells induces the formation of malignant peripheral nerve sheath tumors. These observations suggested that NRG-1 might similarly promote mitogenesis in a variety of neural neoplasms including peripheral neuroepitheliomas, aggressive neural crest-derived neoplasms that arise in nerves and soft tissues. To test this hypothesis, we examined the expression of NRG-1 and its erbB receptors in SK-N-MC neuroepithelioma cells. SK-N-MC cells expressed multiple NRG-1 proteins and mRNAs encoding several alpha and beta isoforms from the sensory and motor neuron-derived factor NRG-1 subfamily as well as the NRG-1 receptor subunits erbB2, erbB3, and erbB4. The erbB receptors expressed by SK-N-MC cells were constitutively tyrosine phosphorylated and inhibiting these kinases with the erbB specific inhibitor PD158780 reduced SK-N-MC DNA synthesis in a dose-dependent manner. We conclude that constitutive activation of the NRG-1/erbB signaling pathway promotes the proliferation of SK-N-MC neuroepithelioma cells in vitro and hypothesize that NRG-1/erbB autocrine, paracrine or juxtacrine signaling may contribute to the development and/or progression of neuroepitheliomas in vivo.     

TLR9 Signaling Promotes Tumor Progression of Human Lung Cancer Cell In Vivo

Toll like receptor 9 (TLR9) was identified mainly in cells of the immune system, and CpG oligonucleotides (CpG ODN), which induces signaling through TLR9, are currently under investigation as adjuvants in clinical therapies against cancer. However, accumulating data suggested that functional TLR9 was also expressed in tumor cells and the effects of TLR9 signaling on the progression of tumor cells remain undefined. Our previous study demonstrated that the TLR9 signaling could significantly enhance the metastatic potential of human lung cancer cells in vitro. Here we carefully evaluated the direct effect of TLR9 signaling on tumor progression of human lung cancer cells in vitro and in vivo. We observed that TLR9 agonist CpG ODN could robustly enhance the tumor progression of 95D cells which expressed high level of TLR9 in nude mice. Furthermore, the CpG ODN could effectively induce the proliferation and IL-10 secretion of 95D cells in vitro. Finally, we demonstrated that CpG ODN could significantly elevate the tumor progression of TLR9 modifying 95C cells in vitro and in vivo, which could be dramatically abrogated by the inhibitory CpG ODN. Our findings indicated that the TLR9 signaling could promote the tumor progression of human tumor cells, which might provide novel insight into the implications for CpG based anti-tumor therapies.     

Interleukin-6-producing Cells in a Human Glioblastoma Cell Line are not Affected by Ionizing Radiation

We investigated the production of interleukin 6 (IL-6) by a radioresistant human glioblastoma cell line G5 after single radiation events of 3, 6 and 9Gy. The total cell number and IL-6 concentration in culture supernatant were assessed 24–96h after irradiation. The radiation impeded or stopped G5 cell growth in a dose-dependent manner, but unexpectedly did not affect the IL-6 concentration in cell culture media that increased in the same range as in non-irradiated cultures. Furthermore, using flow cytometry, we found that the IL-6 positive cells expansion was unaffected by radiation. These findings suggested that this small (about 1%) fraction of G5 cells, constitutively producing IL-6, is highly radioresistant.     

Anti-Migration and Invasion Effects of Astaxanthin against A172 Human Glioblastoma Cell Line

Objectives: The study was to investigate anti-migration and invasion effects of astaxanthin (ATX), a natural carotenoid derivative distributed in marine environments, against A172 human glioblastoma cells. Materials and Methods: Cell viability after ATX treatment was measured by MTT assays. Tumor cell migration and invasion were observed by scratch and Boyden chamber assays, respectively. Expression of MMP-2 and activity of MMP-9 were observed by immunoblotting and gelatin zymography, respectively. Results: ATX up to 150 µM was not toxic to A172 cells at 48 h post-treatment. In contrast, ATX at 50 and 100 µM significantly decreased migration and invasion of A172 cells at 24 and 48 h post-treatment. Metastatic-reducing effect of ATX is associated with the reduction of MMP-2 and MMP-9 expressions in a dose-dependent manner. Conclusion: This finding indicated that ATX has anti-migration and invasion effects against human glioblastoma cells and might be applicable for the protection against metastasis of glioblastoma.     

Radixin Knockdown by RNA Interference Suppresses Human Glioblastoma Cell Growth in Vitro and in Vivo

Radixin, a member of the ERM (ezrin–radixin–moesin) family, plays important roles in cell motility, invasionand tumor progression. It is expressed in a variety of normal and neoplastic cells, including many types ofepithelial and lymphoid examples. However, its function in glioblastomas remains elusive. Thus, in this study,radixin gene expression was first examined in the glioblastoma cells, then suppressed with a lentivirus-mediatedshort-hairpin RNA (shRNA) method.We found that there were high levels of radixin expression in glioblastomaU251cells. Radixin shRNA caused down-regulation of radixin gene expression and when radixin-silenced cellswere implanted into nude mice, tumor growth was significantly inhibited as compared to blank control cells or nonsenseshRNA cells. In addition, microvessel density in the tumors was significantly reduced. Thrombospondin-1(TSP-1) and E-cadherin were up-regulated in radixin- suppressed glioblastoma U251 cells. In contrast, MMP9was down-regulated. Taken together, our findings suggest that radixin is involved in GBM cell migration andinvasion, and implicate TSP-1, E-cadherin and MMP9 as metastasis-inducing factors.     

人肺腺癌吉非替尼获得性耐药株H1975细胞与敏感株PC9细胞miRNA谱表达差异

[目的]分析人肺腺癌吉非替尼耐药细胞株H1975(epidermal growth factor receptor,EGFR基因双突变)和人肺腺癌吉非替尼敏感细胞株PC9(EGFR单突变)细胞株微小RNA(microRNA,miRNA)表达谱的差异.[方法]用Agilent human miRNA芯片分别检测H1975细胞与PC9细胞株的miRNA表达谱,Agilent Feature Extraction软件分析并筛选表达差异达5倍以上的miRNA,生物学软件分析表达差异miRNA的可能靶基因.实时定量PCR(qRT-PCR)验证miRNA芯片结果.[结果]与PC9细胞相比,H1975细胞株中22个miRNA表达上调＞5倍,24个miRNA表达下调＞5倍.qRT-PCR结果验证了芯片的结果(上调的如hsa-miR-489,hsa-miR-210和hsa-miR-21等;下调的如hsa-miR-205,hsa-miR-200c和hsa-miR-155等),同时发现,其中33个异常表达的miRNA有潜在的靶基因,靶基因超过100个的有24个miRNA.[结论]H1975吉非替尼耐药与miRNA谱异常表达有关,miRNA可能通过调控靶基因而参与EGFR-TKI的获得性耐药.     

三氧化二砷对人膀胱癌细胞BIU-87作用的体外研究

目的观察三氧化二砷(arsenic trioxide,As2O3)对人膀胱癌细胞株BIU-87的作用,并探讨其作用机制.方法采用四氮唑蓝(MTT)法检测As2O3不同浓度、不同时间对BIU-87细胞的生长抑制率,同时流式细胞仪检测不同浓度As2O3作用72 h后细胞中与凋亡有关蛋白Fas、Bcl-2的表达.结果As2O3可有效抑制BIU-87细胞的生长,具有浓度、时间依赖性特点.Fas、Bcl-2的表达分别与浓度增加呈正、负相关,P<0.05,且二者随浓度增高呈负相关,P<0.05.结论As2O3可有效抑制膀胱癌细胞生长,其作用机制与凋亡有关.     

Expression Profile of Genes Modulated by Aloe emodin in Human U87 Glioblastoma Cells

Glioblastoma, the most aggressive and malignant form of glioma, appears to be resistant to variouschemotherapeutic agents. Hence, approaches have been intensively investigated to targeti specific molecularpathways involved in glioblastoma development and progression. Aloe emodin is believed to modulate theexpression of several genes in cancer cells. We aimed to understand the molecular mechanisms underlying thetherapeutic effect of Aloe emodin on gene expression profiles in the human U87 glioblastoma cell line utilizingmicroarray technology. The gene expression analysis revealed that a total of 8,226 gene alterations out of 28,869genes were detected after treatment with 58.6 μg/ml for 24 hours. Out of this total, 34 genes demonstratedstatistically significant change (p<0.05) ranging from 1.07 to 1.87 fold. The results revealed that 22 genes wereup-regulated and 12 genes were down-regulated in response to Aloe emodin treatment. These genes were thengrouped into several clusters based on their biological functions, revealing induction of expression of genesinvolved in apoptosis (programmed cell death) and tissue remodelling in U87 cells (p<0.01). Several genes withsignificant changes of the expression level e.g. SHARPIN, BCAP31, FIS1, RAC1 and TGM2 from the apoptoticcluster were confirmed by quantitative real-time PCR (qRT-PCR). These results could serve as guidance forfurther studies in order to discover molecular targets for the cancer therapy based on Aloe emodin treatment.     

慢病毒载体介导RNAi稳定抑制VASH1表达对人脑胶质瘤细胞增殖、凋亡影响的体外研究

目的 探讨运用慢病毒载体介导的RNA干扰技术抑制血管生成抑制因子1（VASH1）的表达对人脑胶质瘤U-87MG细胞增殖和凋亡的影响。方法 应用pGCL-GFP质粒构建针对VASH1的慢病毒shRNA载体,转染入工具细胞293T,筛选出适合浓度的慢病毒转染人脑胶质瘤U-87MG细胞;通过RT-PCR和Western blot评价其对U-87MG细胞内VASH1表达的影响;用四甲基偶氮唑蓝（MTT）法观察U-87MG细胞增殖活性的改变;用流式细胞仪（FCM）检测U-87MG细胞凋亡的变化。结果 与转染阴性对照组和空白组相比,转染pGCL-GFP-VASH1慢病毒载体的U-87MG细胞VASH1的mRNA 蛋白表达水平明显降低（P<0.01）;细胞的增殖活性显著上调（P<0.01）,细胞凋亡明显减少（P<0.01）。结论 VASH1 shRNA慢病毒载体可抑制VASH1在人脑胶质瘤U-87MG细胞中的表达,并增加肿瘤细胞的增殖活性,抑制细胞凋亡。     

溶酶体组织蛋白酶L对人卵巢癌SKOV3细胞迁移及侵袭的作用

目的 探讨溶酶体组织蛋白酶L（Cathepsin L）是否通过上皮-间充质转化（EMT）影响卵巢癌细胞的侵袭及迁移能力。方法 荧光定量PCR法检测人卵巢癌细胞ES-2、SKOV3、OV1以及OV2中CathepsinL的表达水平;设计并合成靶向Cathepsin L的特异性shRNA,通过脂质体转染法转染Cathepsin L表达最高的卵巢癌细胞SKOV3以构建稳定低表达Cathepsin L细胞株,Western blot和定量PCR法验证shRNA的干扰效率;划痕实验及Transwell法检测干扰后细胞的迁移及侵袭能力,Western blot法检测EMT相关指标E-cadherin和N-cadherin以及其上游信号分子Snail、p-AKT的变化。结果 四株卵巢癌细胞中,SKOV3的Cathepsin L表达水平最高（以此为参照）,而ES-2、OV1以及OV2细胞的表达水平分别为0.72±0.04、0.34±0.03和0.55±0.05。Cathepsin L-shRNA转染SKOV3细胞后,SKOV3/shRNA中的Cathepsin L的表达水平较空白组和对照组显著下降;划痕12 h和24 h后, SKOV3/shRNA组的细胞迁移能力明显受到抑制;SKOV3、SKOV3/Con和SKOV3/shRNA组的穿膜细胞数分别为（93.67±8.62）、（90.33±12.22）、（35.67±4.73）,与对照组相比,SKOV3/shRNA组细胞侵袭能力受到显著抑制（P<0.01）;Cathepsin L干扰组细胞的E-cadherin表达增加,N-cadherin的表达降低;此外,Cathepsin L干扰组细胞的Snail、p-AKT表达较对照组显著下降。结论 Cathepsin L可以促进卵巢癌细胞的迁移和侵袭;其机制可能与调节EMT的上游信号分子Snail、p-AKT有关。提示Cathepsin L在卵巢癌的发生发展中起重要作用。     

siRNA介导的survivin基因沉默诱导人膀胱癌BIU-87细胞凋亡的研究

[目的]研究siRNA（small interference RNA）对人膀胱癌BIU-87细胞凋亡和survivin基因表达的影响。[方法]利用Ambion公司设计软件，设计并体外转录合成针对survivin基因的3个特异性siRNA，通过脂质体将siRNA转入BIU-87细胞，分别采用MTT和DNA原位末端标记（TUNEL）法检测siRNA对BIU-87细胞生长抑制率（IR）和凋亡指数（AI），半定量逆转录聚合酶链反应（RT-PCR）和Western Blotting检测siRNA对survivin mRNA及其蛋白表达的影响。[结果]转染后的siRNA1～3组的BIU-87细胞的IR（41.84%、56.21%、54.13%）和AI（21.98%、36.54%、31.34%）均分别显著高于正常对照组（1.98%和3.17%）（P＜0.05），survivin mRNA及其蛋白表达水平均显著低于对照组；其中siRNA2～3对BIU-87细胞的IR、AI和survivin表达的抑制作用均显著高于siRNA1。[结论]体外转录合成的siRNA可抑制BIU-87细胞survivin的表达，诱导BIU-87细胞凋亡，从而抑制BIU-87细胞生长，为siRNA介导的膀胱肿瘤基因沉默提供实验依据。     

Involvement of EGFR,ERK-1,2 and AKT-1,2 Activity on Human Glioma Cell Growth

GBM (Glioblastoma multiforme) is the  most prevalent and lethal primary brain tumor. Gene therapy is one of the promising approaches and  involves the delivery of genetic therapeutic molecules for specific antitumour response/activity. miRNAs can regulate the cell biology functions including replication, cell growth, and apoptosis by regulating gene expression. In this study, we found that down-regulation of miR-4731 expression occurred in GBM cells. We further determined that miR-4731 behaved as a tumor suppressor by inhibiting GBM cell proliferation. We further investigated the molecular mechanisms of miR-4731 and EGFR, ERK-1,2 and AKT-1,2 in GBM cell lines U87 and U251. The in vitro ectopic expression of miR-4731 affected cell proliferation, migration, and invasion of U87 and U251 cells. Luciferase reporter assays validated that miR-4731 targeted the 3′-untranslated region (3′-UTR) of EGFR. In conclusions, we identified that miR-4731 plays a tumor suppressor role in GBM cell proliferation and migration by targeting EGFR expression, and miR-4731 may act as a novel biomarker for early diagnosis or therapeutic target of GBM.     

AntagomiR-27a Targets FOXO3a in Glioblastoma andSuppresses U87 Cell Growth in Vitro and in Vivo

Objective: To study the effect of the antagomiR-27a inhibitor on glioblastoma cells. Methods: The miR-27a expression level in specimens of human glioblastoma and normal human brain tissues excised duringdecompression for traumatic brain injury was assessed using qRT-PCR; The predicted target gene of miR-27awas screened out through bioinformatics databases, and the predicted gene was verified using genetic reportassays; the effect of antagomiR-27a on the invasion and proliferation of glioma cells was analyzed using MTTassays and 5-ethynyl-2’-deoxyuridine (EdU) labeling. A xenograft glioblastoma model in BALB-c nude micewas established to detect the effect of antagomiR-27a on tumour growth. Results: qRT-PCR results showed thatmiR-27a significantly increased in specimens from glioblastoma comparing with normal human brain tissues. ThmiR-27a inhibitor significantly suppressed invasion and proliferation of glioblastoma cells. FOXO3a was verifiedas a new target of miR-27a by Western blotting and reporter analyzes. Tumor growth in vivo was suppressedby administration of the miR-27a inhibitor. Conclusion: MiR-27a may be up-regulated in human glioblastoma,and antagomiR-27a could inhibit the proliferation and invasion ability of glioblastoma cells.