OBJECTIVE:Recurrent high-grade gliomas have a poor prognosis and limited therapeutic options. This study aimed to evaluate the safety and efficacy of SYHA1813, a dual inhibitor of VEGFR and CSF1R, in patients with recurrent high-grade gliomas. METHODS:Eligible patients (aged ≥ 18) with histologically or cytologically confirmed recurrent high-grade gliomas were included. Patients were administered different doses of SYHA1813 daily to assess its safety and initial efficacy. RESULTS:Sixty-four individuals with high-grade gliomas were enrolled. Treatment-related adverse events (TRAEs) were reported in 92.2% of the patients, with 40.6% experiencing grade 3 or higher TRAEs. No grade 5 TRAE was reported. The overall objective response rate (ORR) and disease control rate (DCR) were 18.8% (95% confidence interval [CI], 10.1-30.5) and 51.6% (95% CI, 38.7-64.3), respectively. With a median follow-up duration of 9.5 months, the median progression-free survival (PFS) was 2.8 months (95% CI, 2.3-4.2) with PFS-6 of 22.5% (95% CI, 11.8-35.4) and the median OS was 15.1 months (95% CI, 10.2-NE) with OS-12 of 63.3% (95% CI, 49.3-74.4). Among the 38 patients with glioblastoma, the ORR was 18.4% (95% CI, 7.7-34.3), with a DCR of 52.6% (95% CI, 35.8-69.0). The median PFS and OS were 4.1 months (95% CI, 2.3-5.3) and 13.0 months (95% CI, 9.1-NE), respectively. SYHA1813 was detected in cerebrospinal fluid samples and the drug concentration to plasma free drug concentration ratio was 0.30-1.27. INTERPRETATION:SYHA1813 exhibits encouraging anti-tumor activity with a manageable safety profile for the treatment of recurrent high-grade gliomas, especially glioblastoma. TRIAL REGISTRATION:chictr.org.cn (ChiCTR2100045380).

Background Cerebral ischemia/reperfusion injury can induce nerve cell apoptosis and ferroptosis and activation of the neuroinflammatory cascade plays a critical role in ischemic stroke progression. Mesenchymal stem cells (MSCs) can aid in repairing nerve injuries and regulating inflammatory responses, but their roles in ischemic stroke are unknown. Methods Here, we investigate the impact of microglial susceptibility to ferroptosis on neuronal apoptosis using an oxygen-glucose deprivation/reperfusion (OGD/R) model. Furthermore, we examined the effects of hypoxia-preconditioned olfactory mucosa mesenchymal stem cells (hOM-MSCs) on attenuating microglial ferroptosis and improving neuroinflammatory response in models of OGD/R and middle cerebral artery occlusion (MCAO). Results Firstly, it has been confirmed that the susceptibility of microglial to ferroptosis significantly amplifies their neuroinflammatory response, thereby accelerating neuronal apoptosis in the OGD/R model. A functional assay identified that the core functional factor, peroxisome proliferator-activated receptor-γ co-activator-1α (PGC-1α), secreted from hOM-MSCs has a critical role in the hOM-MSC-modulated recovery of cellular activity in neurons. This discovery was accomplished through inhibiting microglia ferroptosis and the enhancement of immune regulation in the area affected by an infarct, all of which are closely linked to neuroinflammatory reactions. Mechanistically, exposure to hOM-MSCs partially mediates the amelioration of neuroinflammatory response and restoration of neural function in ischemic stroke by means of PGC-1α activation within the infarct region, via initiation of the PPARα-GPX4/ACSL4-NFκB signaling cascades in microglia. Conclusions These findings provide convincing proof that PGC-1α plays a crucial role in facilitating the advantageous impacts of hOM-MSCs on the enhancement of neural functionality following an ischemic stroke. The treatment of hOM-MSC could be a promising and effective neuroprotective candidate to ischemic stroke, and PGC-1α may be used in isolation or in combination with hOM-MSCs for ischemic stroke treatment.

Leptomeningeal metastasis (LM) from lung cancer carries an extremely poor prognosis, with patients often presenting severe intracranial hypertension symptoms such as intractable headache and recurrent vomiting. Ventriculoperitoneal (VP) shunt placement is commonly used to manage intracranial hypertension in leptomeningeal metastasis but carries risks such as infection, shunt malfunction, tumor seeding, abdominal adhesions, or overdrainage. For patients with suspected EGFR L858R/T790M mutations, lumbar cistern drainage offers a safer alternative by draining cerebrospinal fluid (CSF), reducing intracranial pressure (ICP), and preventing sudden death from critical ICP elevation. This approach also provides a critical therapeutic window for EGFR-TKI therapy. Compared to VP shunts, lumbar cistern drainage is preferred due to its minimally invasive nature, fewer procedural complications, and avoidance of general anesthesia. This study reports a case of EGFR L858R/T790M mutation-positive lung adenocarcinoma with LM and life-threatening intracranial hypertension that achieved marked clinical improvement through combined lumbar drainage and furmonertinib therapy. The approach not only facilitated rapid symptom relief and molecular confirmation of EGFR mutation but also enabled sustained disease control.

BACKGROUND:Parkinson's disease (PD) is a neurodegenerative disorder characterized by the degeneration of dopaminergic neurons in the substantia nigra (SN). Activation of the neuroinflammatory response has a pivotal role in PD. Mesenchymal stem cells (MSCs) have emerged as a promising therapeutic approach for various nerve injuries, but there are limited reports on their use in PD and the underlying mechanisms remain unclear. METHODS:We investigated the effects of clinical-grade hypoxia-preconditioned olfactory mucosa (hOM)-MSCs on neural functional recovery in both PD models and patients, as well as the preventive effects on mouse models of PD. To assess improvement in neuroinflammatory response and neural functional recovery induced by hOM-MSCs exposure, we employed single-cell RNA sequencing (scRNA-seq), assay for transposase accessible chromatin with high-throughput sequencing (ATAC-seq) combined with full-length transcriptome isoform-sequencing (ISO-seq), and functional assay. Furthermore, we present the findings from an initial cohort of patients enrolled in a phase I first-in-human clinical trial evaluating the safety and efficacy of intraspinal transplantation of hOM-MSC transplantation into severe PD patients. RESULTS:A functional assay identified that transforming growth factor-β1 (TGF-β1), secreted from hOM-MSCs, played a critical role in modulating mitochondrial function recovery in dopaminergic neurons. This effect was achieved through improving microglia immune regulation and autophagy homeostasis in the SN, which are closely associated with neuroinflammatory responses. Mechanistically, exposure to hOM-MSCs led to an improvement in neuroinflammation and neural function recovery partially mediated by TGF-β1 via activation of the anaplastic lymphoma kinase/phosphatidylinositol-3-kinase/protein kinase B (ALK/PI3K/Akt) signaling pathway in microglia located in the SN of PD patients. Furthermore, intraspinal transplantation of hOM-MSCs improved the recovery of neurologic function and regulated the neuroinflammatory response without any adverse reactions observed in patients with PD. CONCLUSIONS:These findings provide compelling evidence for the involvement of TGF-β1 in mediating the beneficial effects of hOM-MSCs on neural functional recovery in PD. Treatment and prevention of hOM-MSCs could be a promising and effective neuroprotective strategy for PD. Additionally, TGF-β1 may be used alone or combined with hOM-MSCs therapy for treating PD.

Parkinson's disease (PD) is a neurodegenerative disease characterized by the degeneration of dopaminergic neurons in the substantia nigra (SN); the etiology and pathological mechanism of the disease are still unclear. Recent studies have shown that the activation of a neuroimmune response plays a key role in the development of PD. Alpha-synuclein (α-Syn), the primary pathological marker of PD, can gather in the SN and trigger a neuroinflammatory response by activating microglia which can further activate the dopaminergic neuron’s neuroimmune response mediated by reactive T cells through antigen presentation. It has been shown that adaptive immunity and antigen presentation processes are involved in the process of PD and further research on the neuroimmune response mechanism may open new methods for its prevention and therapy. While current therapeutic regimens are still focused on controlling clinical symptoms, applications such as immunoregulatory strategies can delay the symptoms and the process of neurodegeneration. In this review, we summarized the progression of the neuroimmune response in PD based on recent studies and focused on the use of mesenchymal stem cell (MSC) therapy and challenges as a strategy of disease-modifying therapy with multiple targets.

Introduction and importance:Free skin flap transplantation and titanium mesh reconstruction can effectively repair the scalp and skull defects caused by massive scalp tumour resection. Postoperative flap infection is a common complication. Due to the presence of titanium mesh, once infection occurs, a second operation is required to remove the titanium mesh, which brings a great physical and economic burden to the patient.Case presentation:In this case of postoperative infection, the authors used a conservative treatment based on dressing change, preserved the titanium mesh and flap, avoided secondary surgery, and successfully controlled the infection.Clinical discussion:The treatment strategy is mainly divided into three steps: the first stage is to control infection, the authors use complexed iodine to repeatedly disinfect wounds, subcutaneous dead space, exposed titanium mesh, and antibiotic treatment for bacterial culture results; the second stage is to promote granulation growth, After infection control, the authors remove old granulation after each wound disinfection, and then instill fibroblast growth factor to promote subcutaneous granulation growth to fill dead space, and also provide a base platform for epidermal growth; the third stage is mainly epidermal healing, Change the dressing every day to observe the growth of the epidermis.Conclusion:This case suggests that conservative treatment strategy based on dressing change is also a potential treatment option for postoperative infection of the flap with exposure of the titanium plate.

Background The lack of a well-designed brain tumour registry with standardized pathological diagnoses in underdeveloped countries hinders the ability to compare epidemiologic data across the globe. The National Brain Tumour Registry of China (NBTRC), created in January 2018, is the first multi-hospital-based brain tumour registry in China. Patient data reported to the NBTRC in years 2019-2020 were assessed.Methods Tumour pathology was based on the 2016 World Health Organization (WHO) classification of tumours of the central nervous system and ICD-O-3. The anatomical site was coded per the Surveillance, Epidemiology, and End Results (SEER) solid tumour module (version of July 2019). The cases were tabulated by histology and anatomical site. Categorical variables were reported as numbers (percentages). The distribution of tumours by age (0-14, 15-19, 20-39, 40-64, and 65+ years) was analysed.Findings There were a total of 25,537 brain tumours, foremost among them meningioma (23.63%), followed by tumours of the pituitary (23.42%), and nerve sheath tumours (9.09%). Glioblastoma, the most common and lethal form of primary brain cancer in adults, represented 8.56% of all cases. Of note, 6.48% of the malignant tumours were located in the brain stem. The percentage of malignant brain tumours decreased with increasing age, 24.08% in adults (40+ years), 30.25% in young adults (20-39 years), 35.27% in adolescents (15-19 years), and 49.83% in children (0-14 years). Among the 2107 paediatric patients, the most common sites were ventricle (17.19%), brainstem (14.03%), pituitary and craniopharyngeal duct (13.4%), and cerebellum (12.3%), a distribution that differed from that of the entire cohort. The histology distribution was also unique in children, with glioblastoma much less incident compared to the whole cohort (3% vs. 8.47%, p < 0.01). 58.80% of all patients chose higher-level neurosurgical hospitals outside of their province of residence. The median in-hospital length of stay (LOS) for the various pathologies ranged from 11 to 19 days.Interpretation The histological and anatomical site distribution of brain tumours in the NBTRC was statistically different in the subgroup of children (0-14 years). Patient choice of pursuing trans-provincial treatment was common and the in-hospital LOS was longer compared to that reported in similar European and American patient populations, which merits further attention.Funding The National Key Research and Development Program of China (2015BAI12B04, 2013BAI09B03, 2014BAI04B01, and 2021YFF1201104) and Chinese National Natural Science Foundation of China (81971668).Copyright & COPY; 2023 Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license (http:// creativecommons.org/licenses/by-nc-nd/4.0/).

Spinal cord injury (SCI) is a devastating incident that induces neuronal loss and dysfunction. Notoginsenoside R1 (NGR1) has been reported to exhibit a neuroprotective role after SCI. In this study, the effect and molecular mechanisms of NGR1 in models of SCI were further investigated. Rat adrenal pheochromocytoma cell line (PC-12) were stimulated with lipopolysaccharide (LPS) to establish a cell model of SCI-like condition. The changes of proinflammatory cytokines and associated proteins were analyzed using enzyme linked immunosorbent assay (ELISA) and western blotting. A rat model of SCI was established. Nissl staining were used to observe the morphological characteristics of spinal cord tissues. reverse transcription-quantitative PCR (RT-qPCR) was used to measure the expression of miR-301a andKrüppel-like factor 7 (KLF7). Our results showed that NGR1 alleviated LPS-triggered apoptosis and inflammation in PC-12 cells. MiR-301a was upregulated in LPS-stimulated PC-12 cells and was downregulated by NGR1 treatment. MiR-301a overexpression reversed the effect of NGR1 in LPS-treated PC-12 cells. KLF7 was verified to be targeted by miR-301a. NGR1 activated Wnt/β-catenin signaling in LPS-treated PC-12 cells by inhibiting miR-301a and upregulating KLF7. Moreover, blocking wingless/integrated (Wnt)/β-catenin signaling eliminated the protective effect of NGR1 against SCI in vitro and in vivo. Overall, NGR1 could reduce inflammation and apoptosis and promote functional recovery of SCI rats by activating Wnt/β-catenin pathway.

Seizures are a common symptom in glioma patients, and they can cause brain dysfunction. However, the mechanism by which glioma-related epilepsy (GRE) causes alterations in brain networks remains elusive. To investigate the potential pathogenic mechanism of GRE by analyzing the dynamic expression profiles of microRNA/ mRNA/ lncRNA in brain tissues of glioma patients. Brain tissues of 16 patients with GRE and 9 patients with glioma without epilepsy (GNE) were collected. The total RNA was dephosphorylated, labeled, and hybridized to the Agilent Human miRNA Microarray, Release 19.0, 8 × 60 K. The cDNA was labeled and hybridized to the Agilent LncRNA + mRNA Human Gene Expression Microarray V3.0, 4 × 180 K. The raw data was extracted from hybridized images using Agilent Feature Extraction, and quantile normalization was performed using the Agilent GeneSpring. P-value < 0.05 and absolute fold change > 2 were considered the threshold of differential expression data. Data analyses were performed using R and Bioconductor. We found that 3 differentially expressed miRNAs (miR-10a-5p, miR-10b-5p, miR-629-3p), 6 differentially expressed lncRNAs (TTN-AS1, LINC00641, SNHG14, LINC00894, SNHG1, OIP5-AS1), and 49 differentially expressed mRNAs play a vitally critical role in developing GRE. The expression of GABARAPL1, GRAMD1B, and IQSEC3 were validated more than twofold higher in the GRE group than in the GNE group in the validation cohort. Pathways including ECM receptor interaction and long-term potentiation (LTP) may contribute to the disease’s progression. Meanwhile, We built a lncRNA-microRNA-Gene regulatory network with structural and functional significance. These findings can offer a fresh perspective on GRE-induced brain network changes.

BACKGROUND:Accumulating evidence has demonstrated the role of differentially expressed miRNAs in glioma progression. Our previous bioinformatics analyses revealed a role of miR-138-5p in glioma. miR-138-5p was decreased in various tumors, and He et al. found that miR-138-5p had an inhibitory effect on glioma cells in 2021. However, the role of miR-138-5p in the development of glioma and the underlying mechanism is unknown. In this study, we explored whether miR-138-5p affects the biology of glioma by regulating WEE1 expression.METHODS:miR-138-5p and WEE1 G2 checkpoint kinase (WEE1) RNA and protein expression levels in glioma tissues were detected with qRT-PCR and western blotting, respectively. The effects of miR-138-5p and WEE1 on glioma cell migration and invasion were investigated using Transwell assays. CCK-8 assay was used to measure the effects of miR-138-5p and WEE1 on glioma cell proliferation. The mortality of glioma cells transfected with miR-138-5p and WEE1 was measured with flow cytometry. The relationship between miR-138-5p and WEE1 was explored using a luciferase reporter analysis.RESULTS:Functional studies indicated that overexpression of miR-138-5p suppressed cell proliferation, migration, and invasion and promoted death in glioma cell lines. WEE1 was identified as a target of miR-138-5p, and overexpression of miR-138-5p significantly suppressed the levels of WEE1. Moreover, reintroduction of WEE1 partially abrogated miR-138-5p-induced suppression of motility and invasion in glioma cells.CONCLUSION:The low expression of miR-138-5p in glioma suggests a tumor suppressor role for this miRNA. miR-138-5p suppresses glioma progression by regulating WEE1. These data provide new insights into the molecular mechanism of glioma.

Additional file 6: GO analysis of the overlapping target genes

Lung adenocarcinoma (LUAD) is most common pathological type of lung cancer. LUAD with brain metastases (BMs) usually have poor prognosis. To identify the potential genetic factors associated with BM, a genomic comparison for BM cerebrospinal fluid (CSF) and primary lung tumor samples obtained from 1082 early- and late-stage LUAD patients was performed. We found that single nucleotide variation (SNV) of EGFR was highly enriched in CSF (87% of samples). Compared with the other primary lung tissues, copy number gain of EGFR (27%), CDK4 (11%), PMS2 (11%), MET (10%), IL7R (8%), RICTOR (7%), FLT4 (5%), and FGFR4 (4%), and copy number loss of CDKN2A (28%) and CDKN2B (18%) were remarkably more frequent in CSF samples. CSF had significantly lower tumor mutation burden (TMB) level but more abundant copy number variant. It was also found that the relationships among co-occurrent and mutually exclusive genes were dynamically changing with LUAD development. Additionally, CSF (97% of samples) harbored more abundant targeted drugs related driver and fusion genes. The signature 15 associated with defective DNA mismatch repair (dMMR) was only identified in the CSF group. Cancer associated pathway analysis further revealed that ErbB (95%) and cell cycle (84%) were unique pathways in CSF samples. The tumor evolution analysis showed that CSF carried significantly fewer clusters, but subclonal proportion of EGFR was remarkably increased with tumor progression. Collectively, CSF sequencing showed unique genomic characteristics and the intense copy number instability associated with cell cycle disorder and dMMR might be the crucial genetic factors in BM of LUAD.

Glioma is an extremely aggressive malignant neoplasm of the central nervous system. MicroRNA (miRNA) are known to bind to specific target mRNA to regulate post-transcriptional gene expression and are, therefore, currently regarded as promising biomarkers for glioma diagnosis and prognosis. The aim of the present study was to examine the pathogenesis and potential molecular markers of glioma by comparing the differential expression of miRNA and mRNA between glioma tissue and peritumor brain tissue. We explored the impact of screened core miRNA and mRNA on cell proliferation, invasion, and migration of glioma. An miRNA expression profile dataset (GSE90603) and a transcriptome profile dataset (GSE90598) were downloaded from combined miRNA-mRNA microarray chips in the Gene Expression Omnibus (GEO) database. Overall, 59 differentially expressed miRNAs (DEMs) and 419 differentially expressed genes (DEGs) were identified using the R limma software package. FunRich software was used to predict DEM target genes and miRNA-gene pairs, and Perl software was used to find overlapping genes between DEGs and DEM target genes. There were 129 overlapping genes regulated by nine miRNAs between target genes of the DEMs and DEGs. The Chinese Glioma Genome Atlas(CGGA) was analyzed in order to identify miRNAs with diagnostic and prognostic significance. MiR-139-5p, miR-137, and miR-338-3p were validated to be significantly linked to prognosis in glioma patients. Finally, we validated that miR-139-5p affected glioma malignant biological behavior via targeting gamma-aminobutyric acid A receptor alpha 1(GABRA1) through rescue experiments. Low miR-139-5p expression was correlated with survival probability and World Health Organization (WHO) grade. MiR-139-5p overexpression inhibited cell proliferation, migration, and invasion of glioma in vitro. GABRA1 was identified as a functional downstream target of miR-139-5p. Decreased GABRA1 expression was related to similar biological roles as miR-139-5p overexpression while upregulation of GABRA1 effectively reversed the inhibition effects of miR-139-5p. These results demonstrate a novel axis for miR-139-5p/GABRA1 in glioma progression and provide potential prognostic predictors and therapeutic target for glioma patients.

人脯氨酰羟化酶(EGLN)是双加氧酶超家族成员,可直接感受氧分压的变化,是调节缺氧诱导因子(HIF)脯氨酸残基产生羟化降解反应的重要因素,通过影响缺氧诱导因子的转录活性、介导蛋白酶分解和调节亚基的多聚泛素化等发挥作用.近年来,EGLN调节通路和信号机制相关研究的不断深入,为多种疾病的发生、发展及治疗提供了潜在靶点和新的启示.本文拟对EGLN家族在胶质瘤中的研究进展作一综述.

[This corrects the article DOI: 10.3892/ol.2014.2663.].

Additional file 3: GO enrichment of DEMs(BP)

目的 探讨动态对比增强磁共振成像(DCE-MRI)与体素内不相干运动扩散加权成像(IVIM-DWI)在脑胶质瘤术后真、假性进展方面的临床应用价值.方法 选取脑胶质瘤术后同步放化疗后行头部DCE-MRI及IVIM-DWI检查的50例患者.经2次手术病理或随访结果分为脑胶质瘤真性进展(TP)组40例及假性进展(PP)组10例.在放化疗后3个月行MRI平扫及增强,DCE-MRI及IVIM-DWI检查.经后处理获得灌注参数伪彩图、表观扩散系数(ADC)图并计算灌注参数[对比剂从血浆空间渗漏到血管外细胞外的转运常数(Ktrans)、血管外细胞外间隙容积分数(Ve)、速率常数(Kep)、真实扩散系数(D)、灌注相关扩散系数(D?)和灌注分数(f)].采用独立样本t检验,比较胶质瘤TP和PP 2组间的灌注参数,对有统计学意义的参数值做受试者工作特征(ROC)曲线,分别计算敏感度、特异度及曲线下面积(AUC).结果 TP组Ktrans值[(0.118±0.054)min-1 vs(0.039±0.024)min-1]及Ve值(0.282±0.108 vs 0.096±0.066)明显高于PP组,差异有统计学意义(P<0.05),TP组ACD值[(1.229±1.523)×10-3 mm2/s vs(2.257±0.554)×10-3 mm2/s]及f值(0.164±0.095 vs 0.379±0.149)低于PP组(P<0.05).ROC曲线分析,Ktrans值、Ve值、ADC值及f值的AUC分别为0.970、0.921、0.971及0.884,敏感性分别为97.1％、94.3％、100％、80％,特异性分别为93.3％、86.7％、97.1％、88.6％.结论 DCE-MRI及IVIM-DWI可以用于鉴别脑胶质瘤TP与PP,Ktrans值、Ve值、ADC值及f值对二者鉴别具有一定的临床意义.Ktrans值、Ve值、ADC值有良好的诊断效能.

MicroRNAs (miRNAs) refer to a class of small endogenous non-coding RNAs that regulate gene expression at the post-transcriptional level. Emerging studies have shown that miRNAs play critical roles in tumorigenesis and cancer progression. However, roles and mechanisms of miRNA dysregulation in the pathogenesis of meningioma are not fully understood. Here, we first reviewed existing research of aberrantly expressed miRNAs identified by high throughput microarray profiling in meningioma. We also explored the potential of miRNA as biomarkers and therapeutic targets for novel treatment paradigms of meningiomas. In addition, we summarized recent researches that focused on the possible mechanisms involved in miRNA-mediate meningioma occurrence and progression. This review provides an overview of miRNA deregulation in meningioma and indicates the potential of miRNAs to be used as biomarkers or novel therapeutic targets.

Glioma is a highly common malignant brain tumor. Current mainstream treatments include surgery, radiotherapy and chemotherapy, but the low survival rate and poor prognosis of patients have led scientists to explore new therapies. Hyperthermia is a method of local or whole body heating that utilizes high temperature to kill tumor cells to achieve a therapeutic effect, which has multiple advantages in the treatment of glioma, such as minimal invasiveness and high precision, etc. Studies have shown that hyperthermia combined with radiotherapy and chemotherapy can improve the clinical prognosis of patients. Currently, it serves as a therapeutic tool for glioma with huge potential advantages. In this review, the hyperthermia methods applied to treat glioma were introduced. The application prospects and current status of hyperthermia in treating glioma were summarized. In addition, the mature equipment and operation methods that have been applied in the hyperthermia treatment of glioma were illustrated.

MicroRNAs (miRNAs) refer to a class of small endogenous non-coding RNAs that regulate gene expression at the post-transcriptional level. Emerging studies have shown that miRNAs play critical roles in tumorigenesis and cancer progression. However, roles and mechanisms of miRNA dysregulation in the pathogenesis of meningioma are not fully understood. Here, we first reviewed existing research of aberrantly expressed miRNAs identified by high throughput microarray profiling in meningioma. We also explored the potential of miRNA as biomarkers and therapeutic targets for novel treatment paradigms of meningiomas. In addition, we summarized recent researches that focused on the possible mechanisms involved in miRNA-mediate meningioma occurrence and progression. This review provides an overview of miRNA deregulation in meningioma and indicates the potential of miRNAs to be used as biomarkers or novel therapeutic targets.