Malignant cerebral edema after cranioplasty: a case report and literature review.

BACKGROUND: Cranioplasty is a common surgery in the neurosurgery for patients with skull defects following decompression craniectomy. Concomitant rare complications are increasingly reported, such as malignant cerebral edema after cranioplasty. CASE REPORT: A 45-year-old man underwent decompression craniectomy due to traumatic brain injury. At 3 months after the decompression craniectomy, the patient developed refractory subdural hydrogen and received ipsilateral refractory subdural effusion capsule resection, but no significant relief was seen. Therefore, the cranioplasty was decided to treat subdural hydrogen and restore the normal appearance of the skull. After the successful cranioplasty surgery and the expected anesthesia recovery period, the pupils of the patients were continued to be dilated and fixed, without light reflection and spontaneous breathing. The Computed Tomography of the patient 1 hour after surgery showed malignant cerebral edema. CONCLUSIONS: Malignant cerebral edema is a rare and lethal complication after cranioplasty. Negative pressure drainage and deregulation of cerebral blood flow at the end of cranioplasty may partially explain the malignant cerebral after cranioplasty. In addition, patients with epileptic seizures, no spontaneous breathing, dilated pupils without reflection, and hypotension within a short period after cranioplasty may show the occurrence of malignant cerebral.

BHBA treatment improves cognitive function by targeting pleiotropic mechanisms in transgenic mouse model of Alzheimer's disease.

Accumulation of amyloid ß (Aß) peptide, inflammation, and oxidative stress contribute to Alzheimer's disease (AD) and trigger complex pathogenesis. The ketone body ß-hydroxybutyrate (BHBA) is an endogenous metabolic intermediate that protects against stroke and neurodegenerative diseases, but the underlying mechanisms are unclear. The present study aims to elucidate the protective effects of BHBA in the early stage of AD model and investigate the underlying molecular mechanisms. Three-and-half-month-old double-transgenic mice (5XFAD) overexpressing ß-amyloid precursor protein (APP) and presenilin-1 (PS1) were used as the AD model. The 5XFAD mice received 1.5 mmol/kg/d BHBA subcutaneously for 28 days. Morris water maze test, nest construction, and passive avoidance experiments were performed to assess the therapeutic effects on AD prevention in vivo, and brain pathology of 5XFAD mice including amyloid plaque deposition and microglia activation were assessed. Gene expression profiles in the cortexes of 5XFAD- and BHBA-treated 5XFAD mice were performed with high-throughput sequencing and bioinformatic analysis. Mouse HT22 cells were treated with 2 mM BHBA to explore its in vitro protective effects of BHBA on hippocampal neurons against Aß oligomer toxicity, ATP production, ROS generation, and mitochondrial aerobic respiratory function. APP, BACE1, and neprilysin (NEP) expression levels were evaluated in HT22 cells following treatment with BHBA by measuring the presence or absence of G protein-coupled receptor 109A (GPR109A). BHBA improved cognitive function of 5XFAD mice in Morris water maze test, nesting construction and passive avoidance experiments, and attenuated Aß accumulation and microglia overactivation in the brain. BHBA also enhanced mitochondrial respiratory function of hippocampal neurons and protected it from Aß toxicity. The enzymes, APP and NEP were regulated by BHBA via G-protein-coupled receptor 109A (GPR109A). Furthermore, RNA sequencing revealed that BHBA-regulated genes mainly annotated in aging, immune system, nervous system, and neurodegenerative diseases. Our data suggested that BHBA confers protection against the AD-like pathological events in the AD mouse model by targeting multiple aspects of AD and it may become a promising candidate for the prevention and treatment of AD.

Targeting staphylocoagulase with isoquercitrin protects mice from Staphylococcus aureus-induced pneumonia.

Staphylocoagulase (Coa) is a virulence factor of Staphylococcus aureus (S. aureus) that promotes blood coagulation by activating prothrombin to convert fibrinogen to fibrin. Coa plays a crucial role in disease pathogenesis and is a promising target for the treatment of S. aureus infections. Here, we identified that isoquercitrin, a natural flavonol compound, can markedly reduce the activity of Coa at concentrations that have no effect on bacterial growth. Mechanistic studies employing molecular dynamics simulation revealed that isoquercitrin binds to Coa by interacting with Asp-181 and Tyr-188, thereby affecting the binding of Coa to prothrombin. Importantly, in vivo studies showed that isoquercitrin treatment significantly reduced the bacterial burden, pathological damage, and inflammation of lung tissue and improved the percentage of survival of mice infected with S. aureus Newman strain. These data suggest that isoquercitrin is a promising inhibitor of Coa that can be used for the development of therapeutic drugs to combat S. aureus infections.Key Points• Staphylocoagulase plays a key role in the pathogenesis of S. aureus infection.• We identified that isoquercitrin is a direct inhibitor of staphylocoagulase.• Isoquercitrin treatment can significantly attenuate S. aureus virulence in vivo.

Sodium Butyrate Protects N2a Cells against Aß Toxicity In Vitro.

Alzheimer's disease (AD) is a common neurodegenerative disease. Aß plays an important role in the pathogenesis of AD. Sodium butyrate (NaB) is a short-chain fatty acid salt that exerts neuroprotective effects such as anti-inflammatory, antioxidant, antiapoptotic, and cognitive improvement in central nervous system diseases. The aim of this study is to research the protective effects of NaB on neurons against Aß toxicity and to uncover the underlying mechanisms. The results showed that 2 mM NaB had a significant improvement effect on Aß-induced N2a cell injury, by increasing cell viability and reducing ROS to reduce injury. In addition, by acting on the GPR109A receptor, NaB regulates the expression of AD-related genes such as APP, NEP, and BDNF. Therefore, NaB protects N2a cells from Aß-induced cell damage through activating GPR109A, which provides an innovative idea for the treatment of AD.

MiR-592 functions as a tumor suppressor in glioma by targeting IGFBP2.

A growing body of evidence suggests that microRNA-592 is involved in tumor initiation and development in several types of human cancers. However, the biological functions and molecular mechanism of microRNA-592 in glioma remain unclear. In this study, we explored the potential role of microRNA-592 in glioma as well as the possible molecular mechanisms. Our results proved that microRNA-592 expression was significantly downregulated in glioma tissues and cell lines (p < 0.01). Functional assays revealed that overexpression of microRNA-592 dramatically reduced the cell proliferation, migration, and invasion and induced cell arrest at G1/G0 phase in vitro. Mechanistic investigations defined insulin-like growth factor binding protein 2 as a direct and functional downstream target of microRNA-592, which was involved in the microRNA-592-mediated tumor-suppressive effects in glioma cells. Moreover, the in vivo study showed that microRNA-592 overexpression produced the smaller tumor volume and weight in nude mice. In summary, these results elucidated the function of microRNA-592 in glioma progression and suggested a promising application of it in glioma treatment.

Traumatic hemorrhage within a cerebellar dermoid cyst.

Intracranial dermoid cysts with hemorrhage are fairly rare. Herein, we reported a 28-year-old female patient with a cerebellar dermoid cyst, which was found accidently on neuro-imaging after head trauma. MR scanning revealed that the lesion was located within the cerebellar vermis and was measured 3.5cm×3.9cm×3.0cm, with hyper-intensity on T1WI and hypo-intensity on T2WI. However, on CT imaging, it showed hyper-dense signals. It was removed completely via midline sub-occipital approach under surgical microscope. Histological examination proved it was a dermoid cyst with internal hemorrhage. In combination with literature review, we discussed the factors that might be responsible for the hemorrhage within dermoid cysts.

[Retracted] miR­506 functions as a tumor suppressor in glioma by targeting STAT3.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the western blot assay data shown in Figs. 4D, 6B and 7F were strikingly similar to data appearing in different form in other articles by different authors. Furthermore, an independent investigation of this paper conducted by the Editorial Office unveiled possible anomalies associated with the cyclin D1 data presented in Fig. 4D. Owing to the fact that the contentious data in the above article were already under consideration for publication, or had already been published, prior to its submission to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. The authors themselves requested that the paper be retracted. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in Oncology Reports 35: 1057­1064, 2016; DOI: 10.3892/or.2015.4406].

Modulation of lymphatic transport in the central nervous system.

Over the past decade, repeated studies demonstrated that the vertebrate brain had a specialized lymphatic transport pathway, which overturned the traditional concept of central nervous system (CNS) immune privilege. Despite the lack of lymphatic vessels, the glymphatic system and the meningeal lymphatic vessels provide a unique pathway for solutes transport and metabolites clearance in the brain. Sleep, circadian rhythm, arterial pulsation, and other physiological factors modulate this specialized lymphatic drainage pathway. It has also changed significantly under pathological conditions. These modulatory mechanisms may arise critical targets for the therapeutic of CNS disorders. This review highlights the latest research progress on the modulation of lymphatic transport in the CNS under physiological and pathological conditions. Furthermore, we examined the possible upstream and downstream relation networks between these regulatory mechanisms.

[Experimental study on inhibition of retinal neovascularisation by gene transfer of extracellular 1-3 domain of VEGF receptor KDR].

OBJECTIVE: To evaluate the effect of liposome mediated plasmids KDRn3 injected into the vitreous to inhibit experimental retinal neovascularization. METHODS: One-week-old C57BL/6N mice were exposed to 75% ± 2% oxygen for 5 days, then returned to the room air to induce retinal neovascularization. Cationic liposome mediated KDRn3 comp-lex (1 µl) was injected into the vitreous in the treatment group. PBS 1µl or liposome were injected in the control group. The pEGFP-N1/KDRn3 expression was observed by using fluorescence microscope. Retinal neovascularization was evaluated by counting the number of vascular endothelial cell nuclei on the vitreal side of the inner limiting membrane of the retina and measuring the areas of non-perfusions in central retina. RESULTS: KDRn3 protein was expressed both in the ganglion layer and in the inner layer. Retinal wholemount preparation of retinal neovascular animal model showed that prominent neovascular tuft and fluorescein leakage and large areas of non-perfusions in central retina. Fewer neovascular tufts and fewer areas of non-perfusions could be seen after pEGFP-N1/KDRn3 injection. There were statistic differences between control group and pEGFP-N1/KDRn3 injecting group with the number of vascular endothelial cell nuclei on the vitreal side of the inner limiting membrane of the retina (0.20 ± 0.51, 13.58 ± 2.48, 23.05 ± 3.40, 21.70 ± 2.89; F = 1085.25, P < 0.05) and the areas of non-perfusions in central retina [(1.33 ± 0.49), (2.75 ± 0.70), (2.12 ± 0.35) mm(2); F = 17.61, P < 0.01]. CONCLUSION: pEGFP-N1/KDRn3 gene transfer can inhibit retinal neovascularisation in C57Bl/6J mice of ischaemia-induced retinal neovascularisation on some extent.

Current status of infarction in the basal ganglia-internal capsule due to mild head injury in children using PRISMA guidelines.

Post-traumatic basal ganglia-internal capsule (BGIC) infarction in pediatric patients is a relatively rare consequence of mild head injury (MHI). To the best of the authors' knowledge, at present, no comprehensive review has been published. To review research on BGIC infarction after MHI, a literature search was performed using the PubMed database and relevant search terms. According to recent data, MHI may cause BGIC infarction due to mechanical vasospasm of the perforating vessels in pediatric patients. The anatomical characteristics of the growing brain in infancy, mineralization of the lenticulostriate arteries and viral infection may all play a part in BGIC infarction after MHI, which often occurs within 24 months. Symptoms are not as severe and tend to disappear in the early period. Computed tomography or magnetic resonance imaging often shows BGIC infarction. There are also children with scattered calcification of the basal ganglia. Neural rehabilitation is a commonly accepted treatment. The prognosis of patients with BGIC infarction after MHI consistently improves.

The combination of salvianolic acid A with latamoxef completely protects mice against lethal pneumonia caused by methicillin-resistant Staphylococcus aureus.

Staphylococcus aureus (S. aureus), especially methicillin-resistant Staphylococcus aureus (MRSA), is a major cause of pneumonia, resulting in severe morbidity and mortality in adults and children. Sortase A (SrtA), which mediates the anchoring of cell surface proteins in the cell wall, is an important virulence factor of S. aureus. Here, we found that salvianolic acid A (Sal A), which is a natural product that does not affect the growth of S. aureus, could inhibit SrtA activity (IC50 = 5.75 µg/ml) and repress the adhesion of bacteria to fibrinogen, the anchoring of protein A to cell wall, the biofilm formation, and the ability of S. aureus to invade A549 cells. Furthermore, in vivo studies demonstrated that Sal A treatment reduced inflammation and protected mice against lethal pneumonia caused by MRSA. More significantly, full protection (a survival rate of 100%) was achieved when Sal A was administered in combination with latamoxef. Together, these results indicate that Sal A could be developed into a promising therapeutic drug to combat MRSA infections while limiting resistance development.

Baicalein mediates protection against Staphylococcus aureus-induced pneumonia by inhibiting the coagulase activity of vWbp.

The emergence and spread of multidrug-resistant Staphylococcus aureus (S. aureus) necessitate the research on therapeutic tactics which are different from classical antibiotics in overcoming resistance andtreatinginfections. In S. aureus, von Willebrand factor-binding protein (vWbp) is one of the key virulence determinants because it mediates not only the activation of thrombin to convert fibrinogen to fibrin, thereby enabling S. aureus to escape from the host immune clearance, but also the adhesion of S. aureus to host cells. Thus, vWbp is regarded as a promising druggable target to treat S. aureus-associated infections. Here we identify that baicalein, a natural compound isolated from the Chinese herb Scutellaria baicalensis, can effectively block the coagulase activity of vWbp without inhibiting the growth of the bacteria. Through thermal shift and fluorescence quenching assays, we demonstrated that baicalein directly binds to vWbp. Molecular dynamics simulations and mutagenesis assays revealed that the Asp-75 and Lys-80 residues are necessary for baicalein binding to vWbp. Importantly, we demonstrated that baicalein treatment attenuates the virulence of S. aureus and protects mice from S. aureus-induced lethal pneumonia. In addition, baicalein can improve the therapeutic effect of penicillin G by 75% in vivo. These findings indicate that baicalein might be developed as a promising therapeutic agent against drug-resistant S. aureus infections.

Inhibition of autophagy induced by proteasome inhibition increases cell death in human SHG-44 glioma cells.

AIM: The ubiquitin-proteasome system (UPS) and lysosome-dependent macroautophagy (autophagy) are two major intracellular pathways for protein degradation. Recent studies suggest that proteasome inhibitors may reduce tumor growth and activate autophagy. Due to the dual roles of autophagy in tumor cell survival and death, the effect of autophagy on the destiny of glioma cells remains unclear. In this study, we sought to investigate whether inhibition of the proteasome can induce autophagy and the effects of autophagy on the fate of human SHG-44 glioma cells. METHODS: The proteasome inhibitor MG-132 was used to induce autophagy in SHG-44 glioma cells, and the effect of autophagy on the survival of SHG-44 glioma cells was investigated using an autophagy inhibitor 3-MA. Cell viability was measured by MTT assay. Apoptosis and cell cycle were detected by flow cytometry. The expression of autophagy related proteins was determined by Western blot. RESULTS: MG-132 inhibited cell proliferation, induced cell death and cell cycle arrest at G(2)/M phase, and activated autophagy in SHG-44 glioma cells. The expression of autophagy-related Beclin-1 and LC3-I was significantly up-regulated and part of LC3-I was converted into LC3-II. However, when SHG-44 glioma cells were co-treated with MG-132 and 3-MA, the cells became less viable, but cell death and cell numbers at G(2)/M phase increased. Moreover, the accumulation of acidic vesicular organelles was decreased, the expression of Beclin-1 and LC3 was significantly down-regulated and the conversion of LC3-II from LC3-I was also inhibited. CONCLUSION: Inhibition of the proteasome can induce autophagy in human SHG-44 glioma cells, and inhibition of autophagy increases cell death. This discovery may shed new light on the effect of autophagy on modulating the fate of SHG-44 glioma cells.Acta Pharmacologica Sinica (2009) 30: 1046-1052; doi: 10.1038/aps.2009.71.

MiR-17 targets PTEN and facilitates glial scar formation after spinal cord injuries via the PI3K/Akt/mTOR pathway.

OBJECTIVES: We attempted to discover the regulatory role of miR-17 and PTEN in glial scar formation accompanied with spinal cord injuries. METHODS: We established a spinal cord injury (SCI) model in mice which were transfected with different groups of adenoviruses: miR-17 mimics, miR-17 inhibitors and PTEN cDNAs. The improvement of hind limb functions was assessed using the 21-point Basso-Beattie-Bresnahan (BBB) locomotion scale. Immunohistochemistry was used to detect the expression levels of glial fibrillary acidic protein (GFAP), Vimentin and neurofilaments. The expression of miR-17 was quantified using Real time-PCR (RT-PCR). Western blot was conducted to detect the expressions of PTEN, PI3K, Akt, mTOR and S6. Finally, dual luciferase reporter gene assay was conducted to confirm the target relationship between miR-17 and PTEN. RESULTS: The model group exhibited significantly increased expression levels of GFAP, Vimentin, miR-17, PTEN, PI3K, Akt and mTOR. The above trend was enhanced by the transfection of miR-17 mimics (P<0.05). By contrast, the transfection of miR-17 inhibitors significantly down-regulated the expression of GFAP, Vimentin, PTEN, PI3K, Akt, mTOR and p-S6 whereas the expression of GFAP, Vimentin, PI3K, Akt, mTOR and p-S6 in the cells transfected with PTEN cDNAs significantly decreased (P<0.05). Also, the transfection of miR-17 inhibitors and PTEN cDNAs alleviated the astrogliosis in SCI lesions, contributed to the regeneration of nerve filament and improved the functional recovery of the hind limb of mice. Finally, the targeting relationship between miR-17 and PTEN was verified by the dual luciferase reporter gene assay. CONCLUSION: MiR-17 is able to target PTEN and stimulate the PI3K/Akt/mTOR pathway. The formation of glial scar resulted from spinal cord injuries can be reduced either by inhibiting miR-17 or by overexpressing PTEN.

Novel type of peritoneocentesis trocar-assisted distal ventriculoperitoneal shunt placement with supervision via a one-port laparoscope.

Ventriculoperitoneal shunts (VPS) are the primary treatment for hydrocephalus and are associated with a high risk of complications, specifically in patients who are obese or have abdominal adhesions or shunt revisions. The present study describes the use of a novel type of peritoneal catheter peritoneocentesis trocar insertion with the assistance of a one-port laparoscope. A total of 36 patients with hydrocephalus underwent this novel type of peritoneocentesis trocar-assisted VPS. The distal shunt catheter was placed into the right subdiaphragmatic space and the catheter was traversed through a single hole drilled through the liver falciform ligament. The duration of the laparoscopic surgery ranged from 6-18 min (mean 10.4±1.6 min). No shunt-related infections or catheter malfunctions or injuries to the intra-abdominal organs occurred. The total abdominal incision length was 1.0 cm (0.5+0.5 cm). No laparoscopy-related complications were observed during follow-up assessments. The novel approach used in the current study is very easy to perform, and this method may significantly reduce the risk of malfunction complications. The presented method also has the advantages of reduced trauma and a simpler surgery. The current study indicated that this simple, minimally invasive procedure was beneficial for patients with hydrocephalus, specifically in cases of patients with obesity, peritoneal adhesions or shunt revisions.

MiR-506 functions as a tumor suppressor in glioma by targeting STAT3.

MicroRNA-506 (miR-506) has been reported to act as a tumor suppressive or an oncogenic miRNA in different types of tumors. However, the roles and underlying molecular mechanism of miR-506 in glioma remain unclear. In the present study, we performed quantitative PCR to investigate the level of miR-506 in 36 pairs of glioma tumor and matched adjacent tissues, and found that miR-506 was downregulated in the glioma tumors compared to the expression in the adjacent normal tissues. Furthermore, a functional assay found that ectopic expression of miR-506 in glioma cells markedly suppressed cell proliferation, colony formation, migration and invasion, and suppressed tumor growth in vivo. Moreover, signal transducer and activator of transcription 3 (STAT3) was identified as a direct target of miR-506. Western blot assay showed that overexpression of miR-506 not only induced changes in STAT3 expression but also altered expression of its downstream genes, including, Bcl2, cyclin D1 and matrix metalloproteinase 2 (MMP-2), in the human glioma cells. In addition, STAT3 mRNA expression was increased in the glioma tissues, and was inversely correlated with miR-506. Importantly, overexpression of STAT3 in glioma cells attenuated the suppressive effects of miR-506 on cell proliferation, colony formation, migration and invasion. These results showed that miR-506 functions as a tumor suppressor in glioma by targeting STAT3, suggesting that miR-506 may serve as a potential target in the treatment of human glioma.

MicroRNA-141 inhibits glioma cells growth and metastasis by targeting TGF-ß2.

MicroRNA-141 (miR-141) has been reported to function as tumor suppressor in many types of cancer. However, the molecular function and underlying mechanisms of miR-141 in glioma is still unknown. The aims of this study were to investigate miR-141 expression and determine its biological function and underlying mechanism in glioma. In this study, we found that miR-141 expression levels, both in glioma cell lines and in tissues, were significantly lower than that in a normal human astrocyte cell line or adjacent non-cancerous tissues. Overexpression of miR-141 significantly inhibited glioma cell proliferation, colony formation, migration and invasion in vitro, as well as suppressed glioma tumor growth in vivo. In addition, transforming growth factor beta 2 (TGF-ß2) was identified as a target of miR-141 in glioma cells. TGF-ß2 expression was also found to be upregulated, and negatively associated with miR-141 in glioma tissues. TGF-ß2 over-expression partly reversed the effect caused by transfection of miR-141 mimic. These findings together suggested that miR-141 functioned as tumor suppressor by targeting TGF-ß2, and that miR-141 might be a promising therapeutic strategy for future treatment of glioma.

Overexpression of miR-100 inhibits cell proliferation, migration, and chemosensitivity in human glioblastoma through FGFR3.

BACKGROUND: Glioblastoma multiforme is one of the most deadly forms of brain cancer. We investigated the regulatory effects of microRNA-100 (miR-100) on cell proliferation, migration, and chemosensitivity in human glioblastoma. METHODS: miR-100 expression was assessed by quantitative real-time polymerase chain reaction in both glioblastoma cells and human tumors. Lentiviruses of miR-100 mimics and inhibitors were transfected into U251 and T98G cells. The regulatory effects of either overexpressing or downregulating miR-100 on glioblastoma were evaluated by a viability assay, growth assay, migration assay, chemosensitivity assay, and an in vivo tumor transplantation assay. Expression of fibroblast growth factor receptor 3 (FGFR3), the bioinformatically predicted target of miR-100, was examined by Western blot in glioblastoma. FGFR3 was then ectopically overexpressed in U251 and T98G cells, and its effects on miR-100-mediated cancer regulation were evaluated by growth, migration, and chemosensitivity assays. RESULTS: MiR-100 was markedly downregulated in both glioblastoma cell lines and human tumors. Overexpressing miR-100 through lentiviral transfection in U251 and T98G cells significantly inhibited cancer growth (both in vitro and in vivo) and migration and increased chemosensitivity to cisplatin and 1, 3-bis (2-chloroethyl)-l-nitrosourea, whereas downregulation of miR-100 had no effects on development of cancer. FGFR3 was directly regulated by miR-100 in glioblastoma. Ectopically overexpressing FGFR3 was able to ameliorate the anticancer effects of upregulation of miR-100 on glioblastoma growth, migration, and chemosensitivity. CONCLUSION: MiR-100 was generally downregulated in glioblastoma. Overexpressing miR-100 had anticancer effects on glioblastoma, likely through regulation of FGFR3. The MiR-100/FGFR3 signaling pathway might be a biochemical target for treatment in patients with glioblastoma.

MicroRNA-126 acts as a tumor suppressor in glioma cells by targeting insulin receptor substrate 1 (IRS-1).

MicroRNA (miR-126) was reported to be downregulated and to act as a tumor suppressor in cancers of the lung, cervix, bladder, breast, liver and prostate. However, the precise roles and underling mechanisms of miR-126 in glioma remain largely unknown. This study is aimed to study the role of miR-126 in the progression of glioma and to elucidate underlying miR-126-mediated mechanisms in glioma. Our results revealed that miR-126 was downregulated in the collected glioma specimen, compared with non-cancerous brain tissues. Restored miR-126 expression inhibited cell proliferation, colony formation, migration and invasion, and induced cell cycle arrest at G0/G1 phase and cell apoptosis of U-87 MG glioma cells. Overexpression of miR-126 was also able to suppress the growth of U-87 MG glioma xenografts in mice. Furthermore, insulin receptor substrate 1 (IRS-1) were identified as a target of miR-126, and showed that it was negatively regulated by miR-126 in glioma cells. We also demonstrated that overexpression of miR-126 suppressed PI3K and AKT activation, which contribute to suppress tumor growth of glioma. Taken together, these findings showed that miR-126 functions as a tumor suppressor in glioma cells by targeting IRS-1 expression via the PI3K/AKT signaling pathways, suggesting that miR-126 might be a novel target for therapeutic strategies in glioma.