Evaluating the role of DNA methyltransferases in trophoblast fusion and preeclampsia development: Insights from methylation-regulated genes.

The etiology of preeclampsia (PE), a complex and multifactorial condition, remains incompletely understood. DNA methylation, which is primarily regulated by three DNA methyltransferases (DNMTs), DNMT1, DNMT3A, and DNMT3B, plays a vital role in early embryonic development and trophectoderm differentiation. Yet, how DNMTs modulate trophoblast fusion and PE development remains unclear. In this study, we found that the DNMTs expression was downregulated during trophoblast cells fusion. Downregulation of DNMTs was observed during the reconstruction of the denuded syncytiotrophoblast (STB) layer of placental explants. Additionally, overexpression of DNMTs inhibited trophoblast fusion. Conversely, treatment with the DNA methylation inhibitor 5-aza-CdR decreased the expression of DNMTs and promoted trophoblast fusion. A combined analysis of DNA methylation data and gene transcriptome data obtained from the primary cytotrophoblasts (CTBs) fusion process identified 104 potential methylation-regulated differentially expressed genes (MeDEGs) with upregulated expression due to DNA demethylation, including CD59, TNFAIP3, SDC1, and CDK6. The transcription regulation region (TRR) of TNFAIP3 showed a hypomethylation with induction of 5-aza-CdR, which facilitated CREB recruitment and thereby participated in regulating trophoblast fusion. More importantly, clinical correlation analysis of PE showed that the abnormal increase in DNMTs may be involved in the development of PE. This study identified placental DNA methylation-regulated genes that may contribute to PE, offering a novel perspective on the role of epigenetics in trophoblast fusion and its implication in PE development.

Nanorobot-based Direct Implantation of Flexible Neural Electrode for BCI.

Brain-Computer Interface (BCI) has gained remarkable prominence in biomedical community. While BCI holds vast potential across diverse domains, the implantation of neural electrodes poses multifaceted challenges to fully explore the power of BCI. Conventional rigid electrodes face the problem of foreign body reaction induced by mechanical mismatch to biological tissue, while flexible electrodes, though more preferential, lack controllability during implantation. Researchers have explored various strategies, from assistive shuttle to biodegradable coatings, to strike a balance between implantation rigidity and post-implantation flexibility. Yet, these approaches may introduce complications, including immune response, inflammations, and raising intracranial pressure. To this end, this paper proposes a novel nanorobot-based technique for direct implantation of flexible neural electrodes, leveraging the high controllability and repeatability of robotics to enhance the implantation quality. This approach features a dual-arm nanorobotic system equipped with stereo microscope, by which a flexible electrode is first visually aligned to the target neural tissue to establish contact and thereafter implanted into brain with well controlled insertion direction and depth. The key innovation is, through dual-arm coordination, the flexible electrode maintains straight along the implantation direction. With this approach, we implanted CNTf electrodes into cerebral cortex of mouse, and captured standard spiking neural signals.

Orientation Cues-Aware Facial Relationship Representation for Head Pose Estimation via Transformer.

Head pose estimation (HPE) is an indispensable upstream task in the fields of human-machine interaction, self-driving, and attention detection. However, practical head pose applications suffer from several challenges, such as severe occlusion, low illumination, and extreme orientations. To address these challenges, we identify three cues from head images, namely, critical minority relationships, neighborhood orientation relationships, and significant facial changes. On the basis of the three cues, two key insights on head poses are revealed: 1) intra-orientation relationship and 2) cross-orientation relationship. To leverage two key insights above, a novel relationship-driven method is proposed based on the Transformer architecture, in which facial and orientation relationships can be learned. Specifically, we design several orientation tokens to explicitly encode basic orientation regions. Besides, a novel token guide multi-loss function is accordingly designed to guide the orientation tokens as they learn the desired regional similarities and relationships. Experimental results on three challenging benchmark HPE datasets show that our proposed TokenHPE achieves state-of-the-art performance. Moreover, qualitative visualizations are provided to verify the effectiveness of the token-learning methodology.

Knockdown of LMNA inhibits Akt/ß-catenin-mediated cell invasion and migration in clear cell renal cell carcinoma cells.

The LMNA gene encoding lamin A/C is amplified in some clear cell renal cell carcinoma (ccRCC) samples. Our data showed that depletion of the tumor suppressor PBRM1 can upregulate lamin A/C levels, and lamin A/C could interact with PBRM1. However, the role of lamin A/C in ccRCC is not yet fully understood. Our functional assays showed that although the proliferation ability was slightly impaired after LMNA depletion, the migration and invasion of ccRCC cells were significantly inhibited. This suppression was accompanied by a reduction in MMP2, MMP9, AKT/p-AKT, and Wnt/ß-catenin protein levels. Our data therefore suggest that lamin A/C, as an interaction partner of the tumor suppressor PBRM1, plays a crucial role in tumor invasion and metastasis in ccRCC.

Effect of an Emergency Department Process Improvement Package on Suicide Prevention: The ED-SAFE 2 Cluster Randomized Clinical Trial.

Importance: Suicide is a leading cause of deaths in the US. Although the emergency department (ED) is an opportune setting, ED-initiated interventions remain underdeveloped and understudied. Objective: To determine if an ED process improvement package, with a subfocus on improving the implementation of collaborative safety planning, reduces subsequent suicide-related behaviors. Design, Setting, and Participants: The Emergency Department Safety Assessment and Follow-up Evaluation 2 (ED-SAFE 2) trial, a stepped-wedge cluster randomized clinical trial conducted in 8 EDs across the US, used an interrupted time series design with three 12-month sequential phases: baseline, implementation, and maintenance. A random sample of 25 patients per month per site 18 years and older who screened positive on the Patient Safety Screener, a validated suicide risk screener, were included. The primary analyses focused on those who were discharged from the ED, while secondary analyses focused on all patients who screened positive, regardless of disposition. Data were collected on patients who presented for care from January 2014 to April 2018, and data were analyzed from April to December 2022. Interventions: Each site received lean training and built a continuous quality improvement (CQI) team to evaluate the current suicide-related workflow in the ED, identify areas of improvement, and implement efforts to improve. Each site was expected to increase their universal suicide risk screening and implement collaborative safety planning for patients at risk of suicide who were discharged home from the ED. Site teams were centrally coached by engineers experienced in lean CQI and suicide prevention specialists. Main Outcomes and Measures: The primary outcome was a composite comprising death by suicide or suicide-related acute health care visits, measured over a 6-month follow-up window. Results: Across 3 phases, 2761 patient encounters were included in the analyses. Of these, 1391 (50.4%) were male, and the mean (SD) age was 37.4 (14.5) years. A total of 546 patients (19.8%) exhibited the suicide composite during the 6-month follow-up (9 [0.3%] died by suicide and 538 [19.5%] of a suicide-related acute health care visit). A significant difference was observed for the suicide composite outcome between the 3 phases (baseline, 216 of 1030 [21%]; implementation, 213 of 967 [22%]; maintenance, 117 of 764 [15.3%]; P = .001). The adjusted odds ratios of risk of the suicide composite during the maintenance phase was 0.57 (95% CI, 0.43-0.74) compared with baseline and 0.61 (0.46-0.79) compared with the implementation phase, which reflect a 43% and 39% reduction, respectively. Conclusions and Relevance: In this multisite randomized clinical trial, using CQI methods to implement a department-wide change in suicide-related practices, including the implementation of a safety plan intervention, yielded a significant decrease in suicide behaviors in the maintenance period of the study. Trial Registration: ClinicalTrials.gov Identifier: NCT02453243.

PBRM1-deficient PBAF complexes target aberrant genomic loci to activate the NF-κB pathway in clear cell renal cell carcinoma.

PBRM1 encodes an accessory subunit of the PBAF SWI/SNF chromatin remodeller, and the inactivation of PBRM1 is a frequent event in kidney cancer. However, the impact of PBRM1 loss on chromatin remodelling is not well examined. Here we show that, in VHL-deficient renal tumours, PBRM1 deficiency results in ectopic PBAF complexes that localize to de novo genomic loci, activating the pro-tumourigenic NF-κB pathway. PBRM1-deficient PBAF complexes retain the association between SMARCA4 and ARID2, but have loosely tethered BRD7. The PBAF complexes redistribute from promoter proximal regions to distal enhancers containing NF-κB motifs, heightening NF-κB activity in PBRM1-deficient models and clinical samples. The ATPase function of SMARCA4 maintains chromatin occupancy of pre-existing and newly acquired RELA specific to PBRM1 loss, activating downstream target gene expression. Proteasome inhibitor bortezomib abrogates RELA occupancy, suppresses NF-κB activation and delays growth of PBRM1-deficient tumours. In conclusion, PBRM1 safeguards the chromatin by repressing aberrant liberation of pro-tumourigenic NF-κB target genes by residual PBRM1-deficient PBAF complexes.

Bilateral visual loss after selective artery embolization in the neck for hemorrhage of malignant tumor.

INTRODUCTION AND IMPORTANCE: Currently, selective arterial embolization (SAE) has been widely applied for the treatment of many diseases due to its minimal invasiveness. But the complications caused by SAE can be serious. CASE PRESENTATION: Here, we report a case of a patient who experienced bilateral blindness 4 h after selective arterial embolization (SAE). A 67-year-old man, with a 13-year history of nasopharyngeal carcinoma, was admitted to our hospital for nasopharyngeal carcinoma hemorrhage and was scheduled for SAE. The patient did not have any thromboembolic complications. His had a platelet count of 43 × 109/L (range 150-400 × 109/L) and a prothrombin time (PT) of 9.3 s. The surgery was completed under local anesthesia. However, 4 h after the surgery, the patient complained of visual loss. We performed a fundoscopy examination, which showed bilateral ophthalmic artery embolism. CLINICAL DISCUSSION: Bilateral ophthalmic artery embolism is fatal to vision. When this occurs, it would be difficult to save the eyes. So, the relevant selection of the optimal properties of the used PVA and coil embolization materials is important during SAE. CONCLUSION: It is important to improve the existing understanding of the involvement various vessels during embolization of head and neck tumors. Furthermore, special and paramount attention is to be paid to the specific pre-operative angio-architecture, particular patient condition, and the prudent choice of embolic material to prevent the occurrence of ectopic embolization.

Effects of polyol excipient stability during storage and use on the quality of biopharmaceutical formulations.

Biopharmaceuticals are formulated using a variety of excipients to maintain their storage stability. However, some excipients are prone to degradation during repeated use and/or improper storage, and the impurities generated by their degradation are easily overlooked by end users and are usually not strictly monitored, affecting the stability of biopharmaceuticals. In this study, we evaluated the degradation profile of polyol excipient glycerol during repeated use and improper storage and identified an unprecedented cyclic ketal impurity using gas chromatography with mass spectrometry (GC-MS). The other polyol excipient, mannitol, was much more stable than glycerol. The effects of degraded glycerol and mannitol on the stability of the model biopharmaceutical pentapeptide, thymopentin, were also evaluated. The thymopentin content was only 66.4% in the thymopentin formulations with degraded glycerol, compared to 95.8% in other formulations after the stress test. Most glycerol impurities (i.e., aldehydes and ketones) reacted with thymopentin, affecting the stability of thymopentin formulations. In conclusion, this work suggests that more attention should be paid to the quality changes of excipients during repeated use and storage. Additional testing of excipient stability under real or accelerated conditions by manufacturers would help avoid unexpected and painful results.

First detection and molecular identification of Rickettsia massiliae, a human pathogen, in Rhipicephalus sanguineus ticks collected from Southern Taiwan.

The Rickettsia massiliae was firstly detected and identified in Rhipicephalus sanguineus ticks infested on dogs in Taiwan. A total of 1154 Rh. sanguineus ticks collected from 158 dogs of four districts of Tainan city were examined for Rickettsia infection by nested-PCR assay targeting the citrate synthase (gltA) and outer membrane protein B (ompB) genes of Rickettsia. The Rickettsia infection was detected with a general infection rate of 2.77%, and was detected in male, female and nymphal stage with an infection rate of 2.77%, 3.22% and 1.32%, respectively. Phylogenetic relationships were analyzed by comparing the gltA and ompB sequences obtained from 9 Taiwan strains and 16 other strains representing 13 genospecies of Rickettsia. Results revealed that all Taiwan strains were genetically affiliated to the same clades of R. massiliae (spotted fever group) and R. felis (transitional group), and can be discriminated from other genospecies of Rickettsia. This study provides the first evidence of R. massiliae, a pathogenic spotted fever Rickettsia, identified in Rh. sanguineus ticks and highlight the potential threat for the regional transmission of Rickettsia infection among humans in Taiwan.

Study of a High-Temperature and High-Density Water-Based Drilling Fluid System Based on Non-sulfonated Plant Polymers.

The environment-friendly water-based drilling fluid system developed for the petroleum development industry cannot successfully withstand temperatures up to 180 °C, and most high temperature-resistant additives with sulfonic acid groups that have been successfully applied to water-based drilling fluid are not good for environmental protection. In order to solve the above technical problems, a non-sulfonated filtrate reducer and viscosity reducer with resistance to high temperature were prepared by using humic acid, lignin and a multifunctional monomer as raw materials. In laboratory experiments, the molecular weights of the FLO-H filtrate reducer and the VR-H viscosity reducer were 5.45 × 105 g/mol and 8.51 × 103 g/mol, respectively, and all of them showed good high-temperature resistance. The API filtration loss of the bentonite-base slurry with 3.0 wt% FLO-H was only 6.2 mL, which indicated that FLO-H had a prominent reduction in filtration loss after aging at high temperature. When the dosage of VR-H was 1.0 wt%, the plastic viscosity of the water-based drilling fluid after aging at 200 °C decreased from 71 mPa·s to 55 mPa·s, which provided excellent dispersion and dilution. The high-temperature and high-density water-based drilling fluid containing the FLO-H filtrate reducer and the VR-H viscosity reducer had good suspension stability and low filtration performance at the high temperature of 200 °C, which can meet the requirements of high-temperature deep well drilling.

Polymeric Nanohybrids Engineered by Chitosan Nanoparticles and Antimicrobial Peptides as Novel Antimicrobials in Food Biopreservatives: Risk Assessment and Anti-Foodborne Pathogen Escherichia coli O157:H7 Infection by Immune Regulation.

Polymeric nanomaterials (APs) are gaining attention as promising clinical antimicrobials with rapidly increasing antibiotic resistance. Infections by zoonotic enterohemorrhagic Escherichia coli are a severe global threat to public health. Chitosan nanoparticles-microcin J25 (CNM), a class of APs engineered by bioactive peptides and chitosan nanoparticles, can be used as a novel antimicrobial agent against bacterial infections. However, the risk assessment of CNM on animal health or its potential immune modulation to treat serotype E. coli O157:H7 infection impacts in vivo are not well understood. Herein, our findings in mouse models uncovered that oral administration of low levels of CNM significantly increased the body weight and made beneficial effects on the lifespan or clinical signs, accompanied by a significant improvement in gut health, including enhancing the intestinal barrier, immune modulation, and changes in gut microbiota compositions or metabolites. However, high concentrations of CNM induced serious adverse effects, negatively improving intestinal health targets. Anti-infective results proved that oral 0.1% CNM enhances host defense against E. coli O157:H7 infection by improving immune functions and modulating the Th1/Th2 balance. In summary, these findings uncover an instrumental link between the dosage and toxicity risk, suggesting that APs need to be comprehensively assessed for risk before application as safe and reliable food preservatives or therapeutic agents. In addition, CNM as a promising AP may markedly enhance host immunity and therapeutic effects by oral administration.

First detection and molecular identification of a pathogenic spotted fever group Rickettsia, R. massiliae, from Rhipicephalus haemaphysaloides ticks infesting dogs in southern Taiwan.

Tick-borne Rickettsia pathogens become an emerging zoonotic infection worldwide. The prevalence and genetic identity of Rickettsia infection was determined firstly in Rhipicephalus haemaphysaloides ticks collected from dogs in southern Taiwan. A total of 141 Rh. haemaphysaloides ticks were examined for Rickettsia infection by nested-PCR assay targeting the citrate synthase (gltA) and outer membrane protein B (ompB) genes of Rickettsia. The Rickettsia infection was detected with a general infection rate of 2.84%, and was detected in male and female ticks with an infection rate of 3.13% and 2.60%, respectively. Genetic relationships were analyzed by comparing the gltA and ompB sequences obtained from 4 Taiwan strains and 15 other strains representing 13 genospecies of Rickettsia. Phylogenetic analyses reveal that all Taiwan strains were genetically affiliated with the R. massiliae (spotted fever group) and can be distinguished from other genospecies of Rickettsia. These results demonstrate the epidemiological significance of a human pathogenic Rickettsia species (R. massiliae) detected in Rh. haemaphysaloides ticks. Further study focused on the vector competence of this tick species may help to illustrate the potential threat for human infection in southern Taiwan.

PBRM1 deficiency oncogenic addiction is associated with activated AKT-mTOR signalling and aerobic glycolysis in clear cell renal cell carcinoma cells.

The PBRM1 (PB1) gene which encodes the specific subunit BAF180 of the PBAF SWI/SNF complex, is highly mutated (~ 40%) in clear cell renal cell carcinoma (ccRCC). However, its functions and impact on cell signalling are still not fully understood. Aerobic glycolysis, also known as the 'Warburg Effect', is a hallmark of cancer, whether PB1 is involved in this metabolic shift in clear cell renal cell carcinoma remains unclear. Here, with established stable knockdown PB1 cell lines, we performed functional assays to access the effects on 786-O and SN12C cells. Based on the RNA-seq data, we selected some genes encoding key glycolytic enzymes, including PFKP, ENO1, PKM and LDHA, and examined the expression levels. The AKT-mTOR signalling pathway activity and expression of HIF1α were also analysed. Our data demonstrate that PB1 deficiency promotes the proliferation, migration, Xenograft growth of 786-O and SN12C cells. Notably, knockdown of PB1 activates AKT-mTOR signalling and increases the expression of key glycolytic enzymes at both mRNA and protein levels. Furthermore, we provide evidence that deficient PB1 and hypoxic conditions exert a synergistic effect on HIF 1α expression and lactate production. Thus, our study provides novel insights into the roles of tumour suppressor PB1 and suggests that the AKT-mTOR signalling pathway, as well as glycolysis, is a potential drug target for ccRCC patients with deficient PB1.

P2P Lending Default Prediction Based on AI and Statistical Models.

Peer-to-peer lending (P2P lending) has proliferated in recent years thanks to Fintech and big data advancements. However, P2P lending platforms are not tightly governed by relevant laws yet, as their development speed has far exceeded that of regulations. Therefore, P2P lending operations are still subject to risks. This paper proposes prediction models to mitigate the risks of default and asymmetric information on P2P lending platforms. Specifically, we designed sophisticated procedures to pre-process mass data extracted from Lending Club in 2018 Q3-2019 Q2. After that, three statistical models, namely, Logistic Regression, Bayesian Classifier, and Linear Discriminant Analysis (LDA), and five AI models, namely, Decision Tree, Random Forest, LightGBM, Artificial Neural Network (ANN), and Convolutional Neural Network (CNN), were utilized for data analysis. The loan statuses of Lending Club's customers were rationally classified. To evaluate the models, we adopted the confusion matrix series of metrics, AUC-ROC curve, Kolmogorov-Smirnov chart (KS), and Student's t-test. Empirical studies show that LightGBM produces the best performance and is 2.91% more accurate than the other models, resulting in a revenue improvement of nearly USD 24 million for Lending Club. Student's t-test proves that the differences between models are statistically significant.

Construction of a circRNA-Mediated ceRNA Network Reveals Novel Biomarkers for Aortic Dissection.

Background: Aortic dissection (AD) is a rare and lethal disorder with its genetic basis remains largely unknown. Many studies have confirmed that circRNAs play important roles in various physiological and pathological processes. However, the roles of circRNAs in AD are still unclear and need further investigation. The present study aimed to elucidate the underlying molecular mechanisms of circRNAs regulation in AD based on the circRNA-associated competing endogenous RNA (ceRNA) network. Methods: Expression profiles of circRNAs (GSE97745), miRNAs (GSE92427), and mRNAs (GSE52093) were downloaded from Gene Expression Omnibus (GEO) databases, and the differentially expressed RNAs (DERNAs) were subsequently identified by bioinformatics analysis. CircRNA-miRNA-mRNA ceRNA network, Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were used to predict the potential functions of circRNA-associated ceRNA network. RNA was isolated from human arterial blood samples after which qRT-PCR was performed to confirm the DERNAs. Results: We identified 14 (5 up-regulated and 9 down-regulated) differentially expressed circRNAs (DEcircRNAs), 17 (8 up-regulated and 9 down-regulated) differentially expressed miRNAs (DEmiRNAs) and 527 (297 up-regulated and 230 down-regulated) differentially expressed mRNAs (DEmRNAs) (adjusted P-value <0.05 and | log2FC | > 1.0). KEGG pathway analysis indicated that DEmRNAs were related to focal adhesion and extracellular matrix receptor interaction signaling pathways. Simultaneously, the present study constructed a ceRNA network based on 1 circRNAs (hsa_circRNA_082317), 1 miRNAs (hsa-miR-149-3p) and 10 mRNAs (MLEC, ENTPD7, SLC16A3, SLC7A8, TBC1D16, PAQR4, MAPK13, PIK3R2, ITGA5, SERPINA1). qRT-PCR demonstrated that hsa_circRNA_082317 and ITGA5 were significantly up-regulated, and hsa-miR-149-3p was dramatically down-regulated in AD (n = 3). Conclusion: This is the first study to demonstrate the circRNA-associated ceRNA network is altered in AD, implying that circRNAs may play important roles in regulating the onset and progression and thus may serve as potential biomarkers for the diagnosis and treatment of AD.

Effects of polyol excipient stability during storage and use on the quality of biopharmaceutical formulations / 药物分析学报

Biopharmaceuticals are formulated using a variety of excipients to maintain their storage stability.However,some excipients are prone to degradation during repeated use and/or improper storage,and the impurities generated by their degradation are easily overlooked by end users and are usually not strictly monitored,affecting the stability of biopharmaceuticals.In this study,we evaluated the degra-dation profile of polyol excipient glycerol during repeated use and improper storage and identified an unprecedented cyclic ketal impurity using gas chromatography with mass spectrometry(GC-MS).The other polyol excipient,mannitol,was much more stable than glycerol.The effects of degraded glycerol and mannitol on the stability of the model biopharmaceutical pentapeptide,thymopentin,were also evaluated.The thymopentin content was only 66.4％in the thymopentin formulations with degraded glycerol,compared to 95.8％in other formulations after the stress test.Most glycerol impurities(i.e.,aldehydes and ketones)reacted with thymopentin,affecting the stability of thymopentin formulations.In conclusion,this work suggests that more attention should be paid to the quality changes of excipients during repeated use and storage.Additional testing of excipient stability under real or accelerated conditions by manufacturers would help avoid unexpected and painful results.

Lipopolysaccharide induces pyroptosis through regulation of autophagy in cardiomyocytes.

BACKGROUND: Autophagy, a stress response in eukaryotic cells, is closely related to cardiogenic diseases. Pyroptosis, a newly discovered way of programmed cell death, also plays an important role in cardiovascular disease. However, the role and relationship of autophagy and pyroptosis in lipopolysaccharide (LPS)-induced inflammatory response of cardiomyocytes were still unclear. METHODS: Western blot was performed to determine the expression of poly ADP-ribosepolmesera-1 (PARP-1), LC3B, NLRP3 and GSDMD in cardiomyocytes after the treatment of LPS. Transfection of si-LC3B, western blot and immunofluorescence (IF) staining were performed to investigate the role of autophagy in LPS-induced pyroptosis. Co-immunoprecipitation (Co-IP) assays and quantitative real-time PCR (qRT-PCR) were conducted to explore whether PARP-1 binding to LC3B and modulating its expression. Transfections of si-PARP-1, western blot and IF were carried out to confirm the role of PARP-1 in the regulation of LPS-induced pyroptosis by autophagy. RESULTS: LPS induces autophagy and pyroptosis in cardiomyocytes, enhanced the level of autophagy and inhibited the level of pyroptosis in the concentration of 4 µg/mL. We further proved that autophagy inhibits LPS-induced pyroptosis in cardiomyocytes. In addition, PARP-1 binding to LC3B and regulate the expression of LC3B. Finally, we proved that knockdown of PARP-1 rescued the inhibition of autophagy on LPS-induced pyroptosis of cardiomyocytes. CONCLUSIONS: LPS induces pyroptosis through regulation of autophagy via PARP-1 at a specific concentration, above which it causes deposition of autophagy flow to promote pyroptosis. Inhibiting LPS-induced pyroptosis could be a promising therapeutic target in treating cardiovascular diseases.

Identification of miR-21-5p/TET1-negative regulation pair in the aggressiveness of glioma cells.

Increasing evidence highlights that microRNAs (miRNAs) drive glioma initiation and development. Nevertheless, the underlying role of miR-21-5p in glioma is elusive. Hence, we evaluated the underlying role of miR-21-5p in glioma progression. Microarray data analysis provided data indicating that the miR-21-5p level was elevated in glioma. Silenced miR-21-5p suppressed glioma cell growth and invasion. Additionally, our results disclosed that ten-eleven translocation 1 (TET1) was directly targeted by miR-21-5p. Furthermore, antagomir-21-5p restrained glioma cell growth in a xenograft tumour model. In rescue experiments, knockdown of TET1 neutralized miR-21-5p silence-mediated inhibitory function on glioma cell aggressiveness. Taken together, miR-21-5p exerted its carcinogenic effect in glioma cell growth and invasin by targeting TET1.