Search

The widely recommended fracture prediction tool FRAX was developed based on and for the general population. Although several adjusted FRAX methods were suggested for type 2 diabetes (T2DM), they still need to be evaluated in T2DM cohort.This study was undertaken to develop a prediction model for Chinese diabetes fracture risk (CDFR) and compare its performance with those of FRAX.In this retrospective cohort study, 1730 patients with T2DM were enrolled from 2009.08 to 2013.07. Major osteoporotic fractures (MOFs) during follow-up were collected from Electronic Health Records (EHRs) and telephone interviews. Multivariate Cox regression with backward stepwise selection was used to fit the model. The performances of the CDFR model, FRAX, and adjusted FRAX were compared in the aspects of discrimination and calibration.6.3% of participants experienced MOF during a median follow-up of 10 years. The final model (CDFR) included 8 predictors: age, gender, previous fracture, insulin use, diabetic peripheral neuropathy (DPN), total cholesterol, triglycerides, and apolipoprotein A. This model had a C statistic of 0.803 (95%CI 0.761-0.844) and calibration χThe CDFR model has good performance in 10-year MOF risk prediction in T2DM, especially in patients with insulin use or DPN. Future work is needed to validate our model in external cohort(s).

Background A strong relationship between long intergenic non-protein coding RNA 511 (LINC00511) and glioma has been previously reported but the mechanism of LINC00511 in glioma is yet to be determined. This study examined the mechanism of LINC00511 in glioma. Methods The expression of LINC00511 in glioma was determined by bioinformatics analysis and real-time quantitative PCR (RT-qPCR) analysis. The target relationship between genes was predicted by starBase, TargetScan, and was verified by dual-luciferase. Subsequently, siRNA targeting LINC00511 (siLINC00511) and miR-15a-5p mimic were transfected into glioma cells to examine the effect on biological characteristics using cell counting kit-8, clone formation, flow cytometry, wound-healing, and transwell. MiR-15a-5p inhibitor and AEBP1 were used for in vitro rescue experiments, and tumorigenesis assay and immunohistochemical assays were performed for in vivo experiments. Epithelial-mesenchymal transition (EMT) and p65 phosphorylation were examined by Western blot. Results LINC00511 was predicted and verified to be up-regulated in glioma. SiLINC00511 suppressed cell viability, proliferation, migration and invasion, accelerated apoptosis of glioma cells. Mechanically, siLINC00511 promoted E-cadherin expression but suppressed N-cadherin and Snail expressions. MiR-15a-5p bound to LINC00511, and miR-15a-5p inhibitor partially reversed the effect and regulation of siLINC00511 on glioma cells. AEBP1, a target gene of miR-15a-5p, could activate p65 phosphorylation to promote EMT protein expression and partially reverse the inhibitory effect of miR-15a-5p mimic on the malignant phenotype of glioma cells. SiLINC00511 inhibited tumor growth, down-regulated miR-15a-5p expression and up-regulated AEBP1 and Ki67 expressions in vivo. Conclusion LINC00511 knockdown inhibits glioma cell progression via miR-15a-5p/AEBP1 axis.

Glioma is a primary brain tumor with limited treatment approaches and glioblastoma stem cells (GSCs) are manifested with the self-renewal capability and high tumorigenic capacity. This study was performed to investigate the regulatory effect of the SUMO-specific protease 1 (SENP1)/methyltransferase-like 3 (METTL3)/MYC axis on the self-renewal of GSCs mediated by transcription factor Yin Yang 1 (YY1). Following bioinformatics analysis and clinical and cellular experiments, we found that YY1 was highly expressed in GBM tissues and cells, while silencing its expression reduced the self-renewal ability of GSCs. Functionally, YY1 promoted the transcriptional expression of SENP1 by binding to the promoter region of SENP1, while the deSUMOase SENP1 facilitated the methylase activity of m6A through deSUMOylation of the methylase METTL3, thereby promoting the m6A modification of MYC mRNA via METL3 and promoting the expression of MYC. A nude mouse xenograft model of GBM was also constructed to examine the tumorigenicity of GSCs. The obtained findings demonstrated that YY1 promoted tumorigenicity of GSCs by promoting the expression of MYC in vivo. Conclusively, YY1 can transcriptionally upregulate the SUMOylase SENP1 and enhance the methylase activity of METTL3, resulting in the increased m6A modification level of MYC mRNA, thereby promoting the self-renewal of GSCs.

Matrix stiffness is a key physical characteristic of the tumor microenvironment and correlates tightly with tumor progression. Here, we explored the association between matrix stiffness and glioma development. Using atomic force microscopy, we observed higher matrix stiffness in highly malignant glioma tissues than in low-grade/innocent tissues. In vitro and in vivo analyses revealed that culturing glioma cells on stiff polyacrylamide hydrogels enhanced their proliferation, tumorigenesis and CD133 expression. Greater matrix stiffness could obviously up-regulated the expression of BCL9L, thereby promoting the activation of Wnt/β-catenin signaling and ultimately increasing the stemness of glioma cells. Inhibiting Wnt/β-catenin signaling using gigantol consistently improved the anticancer effects of chemotherapy and radiotherapy in mice with subcutaneous glioma tumors. These findings demonstrate that a stiffer matrix increases the stemness of glioma cells by activating BCL9L/Wnt/β-catenin signaling. Moreover, we have provided a potential strategy for clinical glioma treatment by demonstrating that gigantol can improve the effectiveness of traditional chemotherapy/radiotherapy by suppressing Wnt/β-catenin signaling.

Molecular logic computation has drawn extensive attention in the fields of bioanalysis, intelligent diagnostics of diseases and other nanotechnology areas. DNA-templated Au nanoclusters (DNA-AuNCs) possess some excellent features, including high luminescence, good photo-stability and easy preparation. Herein, taking these advantages of DNA-AuNCs, we have designed and constructed a universal platform of label-free and enzyme-free multiple molecular logic gates, including NOR, XNOR, IMPLY, OR, AND, and INHIBIT. The experimental results have demonstrated the feasibility of these logic gates operations using Hg2+, Cu2+, biothiols, melamine and pyrophosphate (PPi) as inputs. Thus, the universal platform can be utilized for the determination of biothiols, melamine and pyrophosphate (PPi) via logic outputs. The strategy exhibited low cost, easy operation and versatile design, and can offer a promising platform for the development of functional logic systems.

Background: Systemic lupus erythematosus (SLE) is an autoimmune disease. Tumor necrosis factor ligand superfamily member 4 (TNFSF4) is an inflammatory factor that has been discussed in different inflammatory diseases and cancers. However, relationship between TNFSF4 and SLE is limited. Material and methods: The present case-control study recruited 400 SLE patients and 600 healthy controls from Southern Chinese Han origin. Plasma levels of TNFSF4 were tested by enzyme linked-immunosorbent assay, and association of rs2205960, rs704840, rs844648, rs3850641 and rs17568 polymorphisms in TNFSF4 gene with SLE risk was evaluated by TaqMan assay according to genotyping.Results: Plasma levels of TNFSF4 were significantly higher in SLE patients than that in healthy controls (390.87 (189.10-906.01) versus 132. 70 (81.27-195.58) pg/ml, P < 0.001). Increased levels of TNFSF4 were positively related to SLE disease activity score, optic nerve injury, leukopenia, and hypocompleminemia. Genotype TT+TG, allele T of rs2205960, genotype GG+GT of rs704840, genotype AA of rs844648 and rs17568 were significantly related to SLE risk (all P < 0.05). Moreover, polymorphism rs844648 was related to SLE patients with clinical feature rash either for genotype AA or allele A.Conclusion: TNFSF4 was elevated in SLE patients and may associate with SLE susceptibility in Southern Chinese Han population.

Chuanhong Zhong,1,2 Bei Tao,3 Yitian Chen,4 Zhangchao Guo,1 Xiaobo Yang,1,2 Lilei Peng,1,2 Xiangguo Xia,1,2 Ligang Chen1,2 1Neurosurgery Department, Affiliated Hospital of Southwest Medical University, Luzhou, People’s Republic of China; 2Neurosurgical Clinical Medical Research Center of Sichuan Province, Luzhou, People’s Republic of China; 3Rheumatism Department, Affiliated Hospital of Southwest Medical University, Luzhou, People’s Republic of China; 4Department of Clinical Medicine, Medical College of Soochow University, Suzhou, People’s Republic of ChinaCorrespondence: Ligang ChenNeurosurgery Department, Affiliated Hospital of Southwest Medical University, Luzhou 646000, People’s Republic of ChinaTel/Fax +86 18113556657Email chenligang199066@163.comPurpose: The aim of this study was to explore the potential role of B7-H3 in malignant glioma progression and identify an innovative approach in clinical glioma therapy.Methods: The protein expression of B7-H3 in high- and low-grade tumor tissues from glioma patients was assessed by immunohistochemistry. The proliferative and invasive ability of B7-H3-overexpressing or knockout glioma cells was analyzed in vitro and in vivo by CCK-8 assay and an orthotopic mouse glioma model, respectively. Activation of the JAK2/STAT3/Slug signaling pathway and epithelial–mesenchymal transition (EMT) was examined by Western blotting and immunofluorescence. The anticancer effects of napabucasin (NAP) and temozolomide (TMZ) were analyzed in an orthotopic mouse glioma model.Results: The expression of B7-H3 was higher in high-grade than in low-grade tumor tissues from glioma patients. In line with this, overexpression of B7-H3 enhanced glioma cell proliferation, induced sustained glioma growth, and promoted glioma cell invasion in vitro and in vivo. Moreover, these effects were mediated through the activation of the JAK2/STAT3/Slug signaling pathway in B7-H3 overexpression glioma cells. We also found that B7-H3 induced EMT processes through downregulation of E-cadherin and upregulation of MMP-2/-9 expression, resulting in enhanced invasion of glioma cells. Finally, we show that the combination of NAP and TMZ significantly suppressed glioma growth and glioma cell invasion, both in vitro and in vivo.Conclusion: B7-H3 overexpression facilitated sustained glioma growth and promoted glioma cell invasion through a JAK2/STAT3/Slug-dependent signaling pathway. Application of the STAT3 inhibitor NAP significantly suppressed glioma growth and invasion, and has potential as a therapeutic strategy for the treatment of glioma.Keywords: B7-H3, glioma, JAK2/STAT3/Slug, temozolomide

Purpose The aim of this study was to explore the potential role of B7-H3 in malignant glioma progression and identify an innovative approach in clinical glioma therapy. Methods The protein expression of B7-H3 in high- and low-grade tumor tissues from glioma patients was assessed by immunohistochemistry. The proliferative and invasive ability of B7-H3-overexpressing or knockout glioma cells was analyzed in vitro and in vivo by CCK-8 assay and an orthotopic mouse glioma model, respectively. Activation of the JAK2/STAT3/Slug signaling pathway and epithelial-mesenchymal transition (EMT) was examined by Western blotting and immunofluorescence. The anticancer effects of napabucasin (NAP) and temozolomide (TMZ) were analyzed in an orthotopic mouse glioma model. Results The expression of B7-H3 was higher in high-grade than in low-grade tumor tissues from glioma patients. In line with this, overexpression of B7-H3 enhanced glioma cell proliferation, induced sustained glioma growth, and promoted glioma cell invasion in vitro and in vivo. Moreover, these effects were mediated through the activation of the JAK2/STAT3/Slug signaling pathway in B7-H3 overexpression glioma cells. We also found that B7-H3 induced EMT processes through downregulation of E-cadherin and upregulation of MMP-2/-9 expression, resulting in enhanced invasion of glioma cells. Finally, we show that the combination of NAP and TMZ significantly suppressed glioma growth and glioma cell invasion, both in vitro and in vivo. Conclusion B7-H3 overexpression facilitated sustained glioma growth and promoted glioma cell invasion through a JAK2/STAT3/Slug-dependent signaling pathway. Application of the STAT3 inhibitor NAP significantly suppressed glioma growth and invasion, and has potential as a therapeutic strategy for the treatment of glioma.

A meta-analysis of eligible studies was performed to evaluate the effectiveness of bone substitute materials (BSMs) in opening wedge high tibial osteotomy (OWHTO) for knee osteoarthritis. A systematic review and meta-analysis were conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA). A comprehensive literature search was performed, and studies comparing BSM with bone graft (BG) and without bone graft (WG) were included. The Cochrane risk of bias tool (version 1.0) and Risk of Bias in Non-randomized Studies of Interventions (ROBINS-I) tool were used to assess the risk of bias for randomized controlled trials (RCTs) and non-randomized studies (NRSs), respectively. The outcomes measured were the osteotomy gap size, the occurrence rates of non-union and lateral hinge fractures, knee functional score, infection and the Visual Analogue Scale (VAS). The quality of evidences was evaluated by Grades of Recommendation, Assessment, Development and Evaluation (GRADE) Working Group system. Five RCTs and eight NRS including 769 participants were included in our meta-analysis. The BSM group had a larger osteotomy gap size than the control group (MD: 0.41 mm, 95% confidence interval (CI): [0.06, 0.76], p=.02, I2=0%), with a significant difference. No significant difference was found between BSM and control group in main analysis in terms of bone non-union, but with a higher non-union rate when BSM combined with long locking plate was used. No significant differences were found in other outcome measures except for VAS from NRS subgroup. The quality of evidence for outcomes was low. BSM combined with locking plate techniques offers a safe and efficient alternative option in OWHTO for osteotomy gap larger than 10 mm, but be aware of the possibility of bone non-union. Given the inherent heterogeneity and low quality of the included studies, future well-designed RCTs are essential to verify the findings.KEY MESSAGEThe treatment of the osteotomy gap is still controversial.BSM combined with a locking plate offers a safe and efficient alternative option for OWHTO with an over 10 mm of osteotomy gap over 10 mm.Due to the inherent heterogeneity and low quality of the included studies, the results should be cautiously interpreted in clinical practice. The treatment of the osteotomy gap is still controversial. BSM combined with a locking plate offers a safe and efficient alternative option for OWHTO with an over 10 mm of osteotomy gap over 10 mm. Due to the inherent heterogeneity and low quality of the included studies, the results should be cautiously interpreted in clinical practice.

BACKGROUND Type 2 diabetes mellitus (T2DM) is associated with a higher fracture risk. Sex hormones are important for maintaining skeletal health. It is not clear which sex hormone(s) contribute(s) to bone mineral density (BMD) and fracture risk in males with T2DM. This study investigated the relationships of these parameters in males with T2DM. METHODS This study involved 482 men with T2DM. BMDs at the lumbar spine (L2-4), femoral neck (FN), and total hip (TH) were measured by dual-energy X-ray absorptiometry (DXA). The 10-year probability of fractures was assessed using the modified Fracture Risk Algorithm (FRAX) tool. Serum levels of sex hormones were measured. RESULTS Follicle-stimulating hormone (FSH) and estradiol (E2) were associated with BMDs at L2-4 (FSH, β = -.162, P < .05; E2, β = .176, P < .001), and E2 was associated with BMD at FN (β = .137, P < .05) and TH (β = .140, P < .05). FSH was associated with major osteoporotic fractures (β = .288, P < .001) and hip fractures (β = .235, P < .001). Higher FSH was a risk factor for osteoporosis/osteopenia (odds ratios [OR] = 2.92, 95% CI = 1.66-5.14, P

Glioma is regarded as an aggressive lethal primary brain tumor. Jumonji domain containing 1C (JMJD1C) is a H3K9 demethylase which participates in the progression of various tumors, but its specific function and underlying mechanism in glioma development remain undefined, which is the purpose of our work. We initially assessed JMJD1C expression in glioma tissues and cells using the assays of RT‐qPCR and immunohistochemistry. Meanwhile, the H3K9 level at the microRNA (miR)‐302a promoter region was measured by chromatin immunoprecipitation assay, while luciferase‐based reporter assay was performed for validation of the binding affinity between miR‐302a and methyltransferase‐like 3 (METTL3). The effect of METTL3 on suppressor of cytokine signaling 2 (SOCS2) was subsequently analyzed by MeRIP‐RT‐qPCR. Finally, a xenograft tumor model was established in nude mice, followed by measurement of tumor‐associated macrophages using flow cytometry. JMJD1C was poorly expressed in glioma tissues. Furthermore, JMJD1C increased miR‐302a expression through promoting H3K9me1 demethylation at the miR‐302a promoter region. miR‐302a was identified to target METTL3, which could inhibit SOCS2 expression via m6A modification. JMJD1C promoted M1 macrophage polarization and suppressed the growth of glioma xenografts through the miR‐302a/METTL3/SOCS2 axis both in vivo and in vitro. In conclusion, JMJD1C could enhance M1 macrophage polarization to inhibit the onset of glioma, bringing a new insight into the contribution of JMJD1C to the pathobiology of glioma, with possible implications for targeted therapeutic method., Our results indicate that JMJD1C enhances M1 macrophage polarization to inhibit the onset of glioma, which brings a new insight for the contributions of JMJD1C to the pathobiology of glioma.

A simple and highly selective fluorescence biosensor has been exploited for p-nitrophenol (p-NP) and alkaline phosphatase (ALP) activity detection based on the glutathione-stabilized copper nanoclusters (GSH-CuNCs) mediated-inner filter effect (IFE). The GSH-CuNCs were prepared by employing GSH as stabilizer and ascorbic acid (AA) as reductant. The obtained GSH-CuNCs exhibited a strong blue fluorescence emission at 420 nm with an excitation wavelength of 365 nm, which overlapped largely with the absorption spectra of p-nitrophenol (p-NP). Therefore, the luminescence of GSH-CuNCs could be quenched by p-NP through inner filter effect. In addition, ALP catalyzed the substrate p-nitrophenyl phosphate (p-NPP) to form p-nitrophenol (p-NP), which also leading to the fluorescence quenching of GSH-CuNCs. The fluorescent strategy was realized for the sensitive determination of p-NP and ALP activity with the promising limit of detection of 20 nM (for p-NP) and 0.003 mU⋅mL

Hydrogen sulfide, a small molecule, produced by endogenous enzymes, such as CTH, CBS, and MPST using L-cysteine as substrates, has been reported to have numerous protective effects. However, the key problem that the target of H

Objective: To summarize the characteristics of patients with pituitary stalk thickening, analyze the association between pituitary stalk width and hypopituitarism, and develop a diagnostic model to differentiate neoplastic and inflammatory origins. Methods: A total of 325 patients with pituitary stalk thickening in a tertiary teaching hospital between January 2012 and February 2018 were enrolled. Basic characteristics and hormonal status were evaluated. Indicators to predict etiology in patients with histologic diagnoses were analyzed. Results: Of the 325 patients, 62.5% were female. Deficiency in gonadotropin was most common, followed by corticotropin, growth hormone, and thyrotropin. The increase in pituitary stalk width was associated with a risk of central diabetes insipidus (odds ratio lOR], 3.57; P Conclusion: Pituitary stalk width could indicate the presence of anterior pituitary dysfunction, especially in central diabetes insipidus patients. With the use of a diagnostic model, the neoplastic and inflammatory causes of pituitary stalk thickening could be preliminarily differentiated. Abbreviations: APD = anterior pituitary dysfunction; AUC = area under the curve; CDI = central diabetes insipidus; GH = growth hormone; MRI = magnetic resonance imaging; OR = odd ratio; PHBS = posterior hypophyseal bright spots; PST = pituitary stalk thickening; PSW = pituitary stalk width

Objective: In kidney diseases, uncontrolled blood pressure, inflammation, oxidative stress, imbalanced immunity response, and metabolic dysfunction were associated with the progressive deterioration of renal function. Short-chain fatty acids (SCFAs), as a group of metabolites fermented by gut microbiota exerted regulatory effects on kidney diseases through their activation of transmembrane G protein-coupled receptors and their inhibition of histone acetylation. In this review article, we updated recent research advances that provided an opportunity to explore our understanding in physiology and function of SCFAs in kidney disease. Data sources: We performed a comprehensive search in both PubMed and Embase using "short-chain fatty acids" and "kidney" with no restrictions on publication date. Study selection: After reading through the title and abstract for early screening, the full text of relevant studies was identified and reviewed to summarize the roles of SCFAs in kidney diseases. Results: Though controversial, growing evidence suggested SCFAs appeared to have a complex but yet poorly understood communications with cellular and molecular processes that affected kidney function and responses to injury. From recent studies, SCFAs influenced multiple aspects of renal physiology including inflammation and immunity, fibrosis, blood pressure, and energy metabolism. Conclusions: The roles of intestinal SCFAs in kidney diseases were exciting regions in recent years; however, clinical trials and animal experiments in kidney diseases were still lacked. Thus, more research would be needed to obtain better understanding of SCFAs’ potential effects in kidney diseases. Key words: Gut microbiome; Short-chain fatty acid; Kidney disease; Gut-kidney axis

Background Parathyroid hormone related protein (PTHrP) triggers white adipose tissue (WAT) browning and cachexia in lung cancer mouse models. It remains unknown whether excessive PTH secretion affects WAT browning and to what extent it contributes to body weight change in primary hyperparathyroidism (PHPT). Methods Using the adeno-associated virus injection, Pth gene over-expressed mice mimicking PHPT were firstly established to observe their WAT browning and body weight alteration. The association between PTH and body weight was investigated in 496 PHPT patients. The adipose browning activities of 20 PHPT and 60 control subjects were measured with PET/CT scanning. Findings Elevated plasma PTH triggered adipose tissue browning, leading to increased energy expenditure, reduced fat content, and finally decreased body weight in PHPT mice. Higher circulating PTH levels were associated with lower body weight (β = −0.048, P = .0003) independent of renal function, serum calcium, phosphorus,and albumin levels in PHPT patients. PHPT patients exhibited both higher prevalence of detectable brown/beige adipose tissue (20% vs 3.3%, P = .03) and increased browning activities (SUV in cervical adipose was 0.77 vs 0.49,P = .02) compared with control subjects. Interpretation Elevated serum PTH drove WAT browning program, which contributed in part to body weight loss in both PHPT mice and patients. These results give insights into the novel pathological effect of PTH and are of importance in understanding the metabolic changes of PHPT. Fund This research is supported by the National Key Research and Development Program of China and National Natural Science Foundation of China.

Objective Up to 40% of multiple endocrine neoplasia type 1 (MEN1) patients may have adrenal cortical tumors. However, adrenocortical carcinoma (ACC) is rare. The clinical manifestations, prevalence, inheritance and prognosis of ACC associated with MEN1 remain unclear. Here we report the clinical manifestations and prevalence of ACC in patients with MEN1. Design and methods A retrospective analysis of ACC associated with MEN1 patients at a single tertiary care center from December 2001 to June 2017. Genetic analysis of MEN1 and other ACC associated genes, loss of heterozygosity (LOH) of MEN1 locus, immunohistochemistry staining of menin, P53 and β-catenin in ACC tissue were performed. Results Two related patients had ACC associated with MEN1. The father had ENSAT stage IV tumor with excessive production of cortisol; the daughter had nonfunctional ENSAT stage I tumor. Both patients carried novel germline heterozygous mutation (c.400_401insC) of MEN1. The wild-type MEN1 allele was lost in the resected ACC tissue from the daughter with no menin staining. The ACC tissue had nuclear β-catenin staining, with heterozygous CTNNB1 mutation of 357del24 and P53 staining in only 20% cells. Conclusions ACC associated with MEN1 is rare and may occur in familial aggregates.

An interesting phenomenon is described that the fluorescence signal of poly(adenine) (A) DNA-templated gold nanoclusters (AuNCs) is greatly improved in the presence of L-histidine by means of L-histidine-DNA interaction. The modified nanoclusters display strong fluorescence emission with excitation/emission maxima at 290/475 nm. The fluorescence quantum yield (QY) is improved from 1.9 to 6.5%. Fluorescence enhancement is mainly ascribed to the L-histidine-DNA interaction leading to conformational changes of the poly(A) DNA template, which offer a better microenvironment to protect AuNCs. The assay enables L-histidine to be determined with good sensitivity and a linear response that covers the 1 to 50 nM L-histidine concentration range with a 0.3 nM limit of detection. The proposed method has been applied to the determination of imidazole-containing drugs in pharmaceutical samples. A turn-on fluorescent method has been designed for the sensitive detection of L-histidine as well as imidazole-containing drugs on the basis of the L-histidine-DNA interaction.

Long non-coding RNAs (lncRNAs) have been manifested to manipulate diverse biological processes, including tumor-induced immune tolerance. Thus, we aimed in this study to identify the expression pattern of lncRNA homeobox A cluster antisense RNA 2 (HOXA-AS2) in glioma and decipher its role in immune tolerance and glioma progression. We found aberrant upregulation of lncRNA HOXA-AS2, lysine demethylase 2A (KDM2A), and jagged 1 (JAG1) and a downregulation of microRNA-302a (miR-302a) in glioma specimens. Next, RNA immunoprecipitation, chromatin immunoprecipitation, and dual-luciferase reporter gene assay demonstrated that lncRNA HOXA-AS2 upregulated KDM2A expression by preventing miR-302a from binding to its 3′untranslated region. The functional experiments suggested that lncRNA HOXA-AS2 could promote regulatory T (Treg) cell proliferation and immune tolerance, which might be achieved through inhibition of miR-302a and activation of KDM2A/JAG1 axis. These findings were validated in a tumor xenograft mouse model. To conclude, lncRNA HOXA-AS2 facilitates KDM2A/JAG1 expression to promote Treg cell proliferation and immune tolerance in glioma by binding to miR-302a. These findings may aid in the development of novel antitumor targets.