Search

IntroductionImproving the quantity and quality of veterinary talent cultivation is an urgent issue to address in current veterinary education and is key to enhancing veterinary talent competitiveness. Starting from an industrial perspective, the introduction of scientific analytical methods for studying veterinary talent competitiveness offers a new view on veterinary education and helps to improve the quality of veterinary education and talent cultivation.MethodsThis study develops a veterinary talent competitiveness evaluation index based on the characteristics of veterinary talent. It proposes a visual method to analyze the level and spatiotemporal evolution of veterinary talent competitiveness using the Entropy method and ArcGIS tools, with Western China as a case study. Data is collected from 12 regions in Western China, spanning 2015 to 2021.ResultsThe results show that the method not only evaluates the current state of veterinary talent competitiveness but also considers temporal and spatial evolution, achieving good evaluation effectiveness and high accuracy, thereby guiding the improvement of veterinary education and talent cultivation.DiscussionBased on the research findings, the study suggests improving the quality of veterinary education and talent cultivation through measures such as strengthening talent resource development, addressing regional imbalances, and promoting spatial integration to achieve a virtuous cycle between veterinary education and industrial development.

Background: Ischemic stroke (IS) is the primary cause of mortality and disability worldwide. Circular RNAs (circRNAs) have been proposed as crucial regulators in IS. This study focused on the role of circPDS5B in IS and its underlying mechanism. Method: Transient middle cerebral artery occlusion (tMCAO) mice and glucose deprivation/reoxygenation (OGD/R)-exposed human brain microvascular endothelial cells (BMECs) were used as IS models. Expression levels of circPDS5B, heterogenous nuclear ribonucleoprotein L (hnRNPL), runt-related transcription factor-1 (Runx1), and Zinc finger protein 24 (ZNF24) were quantified by qRT-PCR. MTT, wound healing, transwell and tube formation assays were employed to evaluate the cell proliferation, migration, and angiogenesis, respectively. Moreover, RNA pull-down, and RIP assay were performed to investigate the interaction among circPDS5B, hnRNPL and vascular endothelial growth factor-A (VEGF-A). Results: circPDS5B was significantly up-regulated in IS patients and tMCAO mice. Deficiency of circPDS5B relieved brain infarction and neuronal injury of tMCAO mice. OGD/R-induced apoptosis, inhibition in viability, migration, and angiogenesis in BMECs were dramatically abrogated by circPDS5B knockdown. Mechanistically, circPDS5B stabilized Runx1 and ZNF24 via recruiting hnRNPL, thereby suppressing the transcription and expression of VEGFA. hnRNPL silencing strengthened circPDS5B knockdown-mediated beneficial effect on IS. Conclusion: Altogether, our study showed that high expression of circPDS5B exacerbated IS through recruitment of hnRNPL to stabilize Runx1/ZNF24 and subsequently inactivate VEGFA. Our findings suggest circPDS5B may be a novel therapeutic target for IS.

Abstract. Meningiomas are the most common primary intracranial neoplasm with diverse pathological types and complicated clinical manifestations. The fifth edition of the WHO Classification of Tumors of the Central Nervous System (WHO CNS5), published in 2021, introduces major changes that advance the role of molecular diagnostics in meningiomas. To follow the revision of WHO CNS5, this expert consensus statement was formed jointly by the Group of Neuro-Oncology, Society of Neurosurgery, Chinese Medical Association together with neuropathologists and evidence-based experts. The consensus provides reference points to integrate key biomarkers into stratification and clinical decision making for meningioma patients. Registration:. Practice guideline REgistration for transPAREncy (PREPARE), IPGRP-2022CN234

Abstract Extracellular vesicles are involved in the occurrence, progression and metastasis of glioblastoma (GBM). GBM can secrete a variety of tumour-derived extracellular vesicles (TDEVs) with high immunosuppressive activity that remotely suppress the systemic immune system, and therapy targeting TDEVs has potential efficacy. In this study, we detected a higher concentration of CD73+ TDEVs enriched in exosomes in central and peripheral body fluids of GBM patients than in those of patients with other brain tumours (low-grade glioma or brain metastases from melanoma or non-small-cell lung cancer). High CD73 expression was detected on the surface of T cells, and this CD73 was derived from TDEVs secreted by GBM cells. In vitro, we observed that CD73+ TDEVs released by GBM cell lines could be taken up by T cells. Moreover, excess adenosine was produced by AMP degradation around T cells and by adenosine receptor 2A (A2AR)-dependent inhibition of aerobic glycolysis and energy-related metabolic substrate production, thereby inhibiting the cell cycle entry and clonal proliferation of T cells. In vivo, defects in exosomal synthesis and CD73 expression significantly inhibited tumour growth in GBM tumour-bearing mice and restored the clonal proliferation of T cells in the central and peripheral regions. These data indicate that CD73+ TDEVs can be used as a potential target for GBM immunotherapy.

Abstract Background New mechanistic insights into the self-renewal ability and multipotent properties of neural stem cells (NSCs) are currently under active investigation for potential use in the treatment of neurological diseases. In this study, NSCs were isolated from the forebrain of fetal rats and cultured to induce NSC differentiation, which was associated with low expression of the non-coding RNA microRNA-335-3p (miR-335-3p). Methods Loss- and gain-of-function experiments were performed in NSCs after induction of differentiation. Results Overexpression of miR-335-3p or FoxM1 and inhibition of the Fmr1 or p53 signaling pathways facilitated neurosphere formation, enhanced proliferation and cell cycle entry of NSCs, but restricted NSC differentiation. Mechanistically, FoxM1 positively regulated miR-335-3p by binding to its promoter region, while miR-335-3p targeted and negatively regulated Fmr1. Additionally, the promotive effect of miR-335-3p on NSC self-renewal occurred via p53 signaling pathway inactivation. Conclusion Taken together, miR-335-3p activated by FoxM1 could suppress NSC differentiation and promote NSC self-renewal by inactivating the p53 signaling pathway via Fmr1.

BackgroundColorectal surgery is associated with a high risk of surgical site infection (SSI). In March 2017, we developed an intervention, called “PRESS”, with the aim of reducing colorectal superficial SSI. This study assessed the effect of the new intervention in reducing the rates of superficial SSI in colorectal surgery.MethodsThis study was a retrospective review of 312 PRESS+ patients compared to 171 historical control PRESS− patients who were 18 years of age or older and underwent elective colorectal surgery with clean-contaminated wounds from January 2015 to June 2020. In the PRESS+ groups, we pressed the incision downward hard with clean gauze after the interrupted suturing of the skin. Propensity score matching with 15 variables was performed in a 1:1 ratio to reduce selection bias. Univariate analysis and multivariate analysis were performed to identify risk factors associated with SSI.ResultsThe characteristics of the PRESS+ (n = 160) and PRESS− (n = 160) groups were well balanced after propensity score matching. The PRESS+ group had a lower superficial SSI rate (1.9% vs. 6.9%, P = 0.029) and a lower overall SSI rate (2.5% vs. 10.0%, P = 0.006) than the PRESS− group. Furthermore, multivariate analysis showed that the incisional press was an effective protective factor for superficial SSI (adjusted odds ratio = 0.215, 95% confidence interval = 0.057–0.818, P = 0.024). In addition, female sex (P = 0.048) and blood transfusion (P = 0.011) were demonstrated to be independent risk factors for superficial SSI.ConclusionThe incisional press after suturing is a simple, costless, and effective intervention in reducing superficial incisional SSI.

Abstract Background LncRNA was known to be closely associated with the progression of human tumors. The role of lncRNA LIFR-AS1 in the pathogenesis and progression of gastric tumor is still unclear. The aim of this study was to investigate the function of LIFR-AS1 and the underlying mechanism in the pathogenesis and progression of gastric cancer. Methods QRT-PCR was used to evaluate the expression of LIFR-AS1, miR-29a-3p and COL1A2 in gastric tumor tissues and cells. Western blotting was used to evaluate the protein expression of COL1A2 in gastric tumor cells. CCK-8 assay, transwell assay and flow cytometry were used to evaluate the roles of LIFR-AS1, miR-29a-3p and COL1A2 in cell proliferation, invasion, migration and apoptosis. The relationship among LIFR-AS1, miR-29a-3p and COL1A2 was assessed by bioinformatics analyses and luciferase reporter assay. Results The expression levels of LIFR-AS1 were significantly increased in gastric tumor tissues and cells, while the expression levels of miR-29a-3p were decreased. The expression of miR-29a-3p was negatively correlated with the expression of LIFR-AS1 in gastric cancer tumor tissues. Knocking down of LIFR-AS1 inhibited proliferation, invasion and migration of gastric tumor cells, and induced apoptosis of gastric tumor cells. Bioinformatics analyses and integrated experiments revealed that LIFR-AS1 elevated the expression of COL1A2 through sponging miR-29a-3p, which further resulted in the progression of gastric tumor. Conclusion LIFR-AS1 plays an important role as a competing endogenous RNA in gastric tumor pathogenesis and may be a potential target for the diagnosis and treatment of gastric tumor.

Abstract Background 17AAG has been extensively studied for its antitumor effects that protect cells from lethal stress by maintaining protein stability. The role of 17AAG in sevoflurane-induced neuronal injury has never been studied. We aim to investigate the effect of 17AAG on sevoflurane-induced neurotoxicity in vivo and in vitro. Methods Sevoflurane-induced hippocampal neuron injury model was established in aged Sprague–Dawley rats. Pretreatment of vehicle or 17AAG was administered prior to sevoflurane inhalation. H4 neuroglioma cells were pretreated with vehicle or 17AAG and exposed to sevoflurane. Apoptosis, oxidative stress, expression of interleukin-6 (IL-6), and activation of the nuclear factor-κB (NF-κB) signaling pathway in H4 cells were examined by Hoechst assay, flow cytometry, Western blot, and immunofluorescent staining. RNA interference against HSPA1A was performed to test the function of HSP70 in neuroprotection. Results Exogenous 17AAG reduced sevoflurane-induced apoptosis and oxidative stress in rat hippocampal neurons and in H4 cells. In H4 cells, 17AAG suppressed sevoflurane-induced upregulation of IL-6 and activation of NF-κB signaling. 17AAG enhanced sevoflurane-induced upregulation of HSP70 in rat hippocampal neurons and in H4 cells. Conversely, silencing of HSPA1A in H4 cells blocked the cytoprotective effect of 17AAG against sevoflurane-induced apoptosis and oxidative stress, and prevented upregulation of IL-6 and activation of NF-κB signaling. Conclusions 17AAG protects against sevoflurane-induced neurotoxicity in vivo and in vitro via HSP70-dependent inhibition of apoptosis, oxidative stress, and pro-inflammatory signaling pathway.

Objective: Glioblastoma (GBM) is the most frequent brain malignancy with high incidence, and long noncoding RNAs (lncRNAs) exerts functions in GBM. In this research, we focused on the capabilities of lncRNA RBPMS-AS1 in radiosensitivity of GBM. Methods: RBPMS-AS1 and CAMTA1 expression levels were determined in GBM tissues and cells. StarBase v3.0 database was searched for predicting miRNAs that simultaneously bound to RBPMS-AS1 and CAMTA1. pcDNA3.1-RBPMS-AS1, pcDNA3.1-CAMTA1, miR-301a-3p mimic, or pcDNA3.1-RBPMS-AS1/pcDNA3.1-CAMTA1 and miR-301a-3p mimic were transfected into GBM cells to test radiosensitivity, cell proliferation and apoptosis. The interactions of miR-301a-3p with RBPMS-AS1 and CAMTA1, as well as CAMTA1 and NRGN, were confirmed. In vivo imaging technology was utilized to detect tumor growth in orthotopic xenograft tumors, and Ki67 expression was tested in intracranial tumors. Results: RBPMS-AS1 and CAMTA1 levels were reduced in GBM tissues and cells. miR-301a-3p had a binding site with both RBPMS-AS1 and CAMTA1 and it was the most significantly-upregulated one. Upregulation of RBPMS-AS1 or CAMTA1 enhanced the radiosensitivity and cell apoptosis while suppressing proliferation of GBM cells. Conversely, miR-301a-3p overexpression diminished the radiosensitivity and cell apoptosis while inducing proliferation of GBM cells. Overexpression of RBPMS-AS1 or CAMTA1 reversed the effects of overexpressed miR-301a-3p in GBM cells. Mechanistically, RBPMS-AS1 enhanced CAMTA1 expression in GBM cells through sponging miR-301a-3p, and CAMTA1 promoted NRGN expression. In animal experiments, overexpressed RBPMS-AS1 inhibited tumor growth and the positive expression of Ki67 both before and after radiation therapy. Conclusion: RBPMS-AS1 promotes NRGN transcription through the miR-301a-3p/CAMTA1 axis and enhances the radiosensitivity of GBM.

Cognitive impairment is associated with aging; however, the underlying mechanism remains unclear. Our previous study found that polyphenol-rich blueberry–mulberry extract (BME) had an antioxidant capability and effectively alleviated cognitive impairment in a mouse model of Alzheimer’s disease. Thus, we hypothesized that BME would improve cognitive performance in naturally aging mice and assessed its effects on related signaling pathways. Eighteen-month-old C57BL/6J mice were gavaged with 300 mg/kg/d of BME for 6 weeks. Behavioral phenotypes, cytokine levels, tight junction protein levels, and the histopathology of the brain were assessed, and 16S ribosomal RNA sequencing and targeted metabolome analyses were used for gut microbiota and metabolite measurements. Our results showed that the cognitive performance of aged mice in the Morris water maze test was improved after BME treatment, neuronal loss was reduced, IL-6 and TNF-α levels in the brain and intestine were decreased, and the levels of intestinal tight junction proteins (ZO-1 and occludin) were increased. Further, 16S sequencing showed that BME significantly increased the relative abundance of Lactobacillus, Streptococcus, and Lactococcus and decreased the relative abundance of Blautia, Lachnoclostridium, and Roseburia in the gut. A targeted metabolomic analysis showed that BME significantly increased the levels of 21 metabolites, including α-linolenic acid, vanillic acid, and N-acetylserotonin. In conclusion, BME alters the gut microbiota and regulates gut metabolites in aged mice, which may contribute to the alleviation of cognitive impairment and to inflammation inhibition in both the brain and the gut. Our results provide a basis for future research on natural antioxidant intervention as a treatment strategy for aging-related cognitive impairment.

ObjectiveTo investigate the differential expression of lncRNA in glioma cells, as well as the effect of lncRNA NKX3-1 on glioma cells.MethodsGlioma-related data were first downloaded from the TCGA database and analyzed using bioinformatics, after which the lncRNA NKX3-1 was chosen for further experiments. The expression of the lncRNA NKX3-1 in glioma tumor samples was detected using qRT-PCR. The subcellular localization of lncRNA NKX3-1 was determined using fluorescence in situ hybridization (FISH). CCK-8, flow cytometry, cell scratch, and transwell assays were used to detect cell proliferation, apoptosis, and invasion. The downstream pathway of lncRNA NKX3-1 was investigated using luciferase assays and detected using western blot, transwell, and cell scratch assays.ResultsThe differential expression profile of lncRNA in glioma was obtained. NKX3-1 lncRNA was found to be significantly increased in glioma tumor tissues. LncRNA NKX3-1 was found in the nucleus. Proliferation, invasion, and migration of glioma cells were significantly increased (P

Alzheimer’s disease (AD) is a neurodegenerative disease characterized by amyloid plaques and neurofibrillary tangles which significantly affects people’s life quality. Recently, AD has been found to be closely related to autophagy. The aim of this study was to identify autophagy-related genes associated with the pathogenesis of AD from multiple types of microarray and sequencing datasets using bioinformatics methods and to investigate their role in the pathogenesis of AD in order to identify novel strategies to prevent and treat AD. Our results showed that the autophagy-related genes were significantly downregulated in AD and correlated with the pathological progression. Furthermore, enrichment analysis showed that these autophagy-related genes were regulated by the transcription factor myocyte enhancer factor 2A (MEF2A), which had been confirmed using si-MEF2A. Moreover, the single-cell sequencing data suggested that MEF2A was highly expressed in microglia. Methylation microarray analysis showed that the methylation level of the enhancer region of MEF2A in AD was significantly increased. In conclusion, our results suggest that AD related to the increased methylation level of MEF2A enhancer reduces the expression of MEF2A and downregulates the expression of autophagy-related genes which are closely associated with AD pathogenesis, thereby inhibiting autophagy.

We have reported that transient receptor potential melastatin-related 7 (TRPM7) regulates glioma stem cells (GSC) growth and proliferation through Notch, STAT3-ALDH1, and CD133 signaling pathways. In this study, we determined the major contributor(s) to TRPM7 mediated glioma stemness by further deciphering each individual Notch signaling. We first determined whether TRPM7 is an oncotarget in glioblastoma multiforme (GBM) using the Oncomine database. Next, we determined whether TRPM7 silencing by siRNA TRPM7 (siTRPM7) induces cell growth arrest or apoptosis to reduce glioma cell proliferation using cell cycle analysis and annexin V staining assay. We then examined the correlations between the expression of TRPM7 and Notch signaling activity as well as the expression of GSC markers CD133 and ALDH1 in GBM by downregulating TRPM7 through siTRPM7 or upregulating TRPM7 through overexpression of human TRPM7 (M7-wt). To distinguish the different function of channel and kinase domain of TRPM7, we further determined how the α-kinase-dead mutants of TRPM7 (α-kinase domain deleted/M7-DK and K1648R point mutation/M7-KR) affect Notch activities and CD133 and ALDH1 expression. Lastly, we determined the changes in TRPM7-mediated regulation of glioma cell growth/proliferation, cell cycle, and apoptosis by targeting Notch1. The Oncomine data revealed a significant increase in TRPM7 mRNA expression in anaplastic astrocytoma, diffuse astrocytoma, and GBM patients compared to that in normal brain tissues. TRPM7 silencing reduced glioma cell growth by inhibiting cell entry into S and G2/M phases and promoting cell apoptosis. TRPM7 expression in GBM cells was found to be positively correlated with Notch1 signaling activity and CD133 and ALDH1 expression; briefly, downregulation of TRPM7 by siTRPM7 decreased Notch1 signaling whereas upregulation of TRPM7 increased Notch1 signaling. Interestingly, kinase-inactive mutants (M7-DK and M7-KR) resulted in reduced activation of Notch1 signaling and decreased expression of CD133 and ALDH1 compared to that of wtTRPM7. Finally, targeting Notch1 effectively suppressed TRPM7-induced growth and proliferation of glioma cells through cell G1/S arrest and apoptotic induction. TRPM7 is responsible for sustained Notch1 signaling activation, enhanced expression of GSC markers CD133 and ALDH1, and regulation of glioma stemness, which contributes to malignant glioma cell growth and invasion.

Abstract Glioma is the most common intracranial malignant tumors, accounting for about 40% of intracranial tumors. Primary or secondary drug resistance is one of the main reasons for the failure of treatment. The oncogenic or tumor‐suppressive roles of miR‐634 have been revealed in different types of cancer. However, the role of miR‐634 in glioma remains unknown and whether miR‐634 could sensitize glioma cells to temozolomide also is unclear. Here, we aim to investigate the biological function of miR‐634 and the possible mechanisms in glioma. In this study, we found that miR‐634 was downregulated in glioma tissues compared with normal brain tissues, and its expression was associated with tumor size and WHO grade. Importantly, glioma patients with low miR‐634 expression showed a shorter survival time than patients which had high expression of miR‐634. This study also showed that miR‐634 was decreased in temozolomide‐resistant glioma cells, and restoration of miR‐634 could sensitize the resistant cells to temozolomide by targeting CYR61 through Raf‐ERK signaling. Our study provides a potential target for overcome drug resistance in glioma.

Background: as the most common malignancy of the central nervous system, low-grade glioma (LGG) patients suffered a poor prognosis. Tumor microenvironment, especially immune components, plays an important role in the progression of tumors. Thus, it is critical to explore the key immune-related genes, a comprehensive understanding of the TME in LGG helps us find novel cancer biomarkers and therapeutic targets. Methods: the GPSM3 expression level and the correlations between clinical characteristics and GPSM3 levels were analyzed with the data from CGGA and TCGA dataset. Univariate and multivariate cox regression model were built to predict the prognosis of LGG patients with multiple factors. Then the correlation between GPSM3 with immune cell infiltration was explored by ESTIMATE, CIBERSORT and TIMER2.0. At last, the correlation analyzed between GPSM3 expression and immune checkpoint related genes were also analyzed. Results: GPSM3 expression was overexpressed in LGG and negatively correlated to the GPSM3 DNA methylation. Univariate and multivariate Cox analysis demonstrated that GPSM3 expression was an independent prognostic factor in LGG patients. Functional characterization of GPSM3 revealed that it was associated with many immune processes to tumor cells. GPSM3 expression was positive related to the immune score, Stromal scores and ESTIMATE scores, but negative related to the Tumor purity. Immune features in the TME of GPSM3-high LGG group is characterized by a higher infiltrating of regulatory T cells, neutrophils, macrophages M2, and a lower proportion of monocytes than to the GPSM3-low group. Furthermore, GPSM3 expression exhibited significant correlations with the immune checkpoint-related genes, especially PD-1, PD-L1, PD-L2, CTLA4 and TIM3. Conclusions: these findings proved that GPSM3 could serve as a prognostic biomarker and potential immunotherapy target for LGG.

Abstract The aim of this study was to compare the outcomes of laparoscopic surgery (LAP) and open gastric surgery (OP) in early gastric cancer patients aged ≥70 years.We conducted a retrospectively analysis among patientswith pathological T1N0M0 gastric cancer,who underwent LAP or OP between January 1, 2001 and December 31, 2008. We identified a well-balanced cohort of 2,360 patients (1180 patients in each group). LAP has been shown to offer a superior perioperative results to OP, including lower blood loss, shorter time to oral intake, walk and bowel function recovery, shorter time of hospital stay, and less blood transfusion required. However, the intraoperative and postoperative complications, local recurrence, and metastasis didn’t show statistically significant differences between groups. The 5-year overall survival (OS), disease-free survival (DFS), and cancer-specific survival (CSS) were 60.1% vs.63.2%, 80.8% vs. 83.3%, and 87.6% vs. 89.5% in the LAP group and OP group, respectively. The hazard ratios (HR) for OS, DFS, and CSS were 1.09(95% confidence interval [CI]: 0.95–1.25; P = 0.215), 1.03(95% CI: 0.91–1.18; P = 0.636), and 1.07 (95% CI: 0.88–1.30; P = 0.484), respectively, compared LAP group with OP group. In conclusion, LAP is an acceptable alternative to OP in elderly patients with early gastric cancer.

Background. Bone marrow-derived mesenchymal stem cells (BMSCs) have blossomed into an effective approach with great potential for the treatment of liver fibrosis. The aim of this study was to investigate the underlying antifibrosis mechanisms by which the BMSC inhibit activated hepatic stellate cells (HSCs) in vivo and in vitro. Methods. To study the effect of human bone marrow-derived mesenchymal stem cells (hBM-MSCs) on activated HSCs, we used HSCs and the coculture systems to evaluate the inhibition of activated HSCs from the aspects of the apoptosis of activated HSCs. In addition, activation of NADPH oxidase pathway and the changes in liver histopathology were tested by using the carbon tetrachloride- (CCl4-) induced liver fibrosis in mice. Results. Introduction of hBM-MSCs significantly inhibited the proliferation of activated HSCs by inducing the apoptosis process of activated HSCs. The effect of hBM-MSCs reduced the signaling pathway of NADPH oxidase in activated HSCs. Besides, the signaling pathway of NADPH oxidase mediated hBM-MSC upregulation of the expression of the peroxisome proliferator-activated receptor γ and downregulation of the expression of α1(I) collagen and alpha-smooth muscle actin (α-SMA) in activated HSCs. Moreover, the hBM-MSC-induced decrease in the signaling pathway of NADPH oxidase was accompanied by the decrease of the activated HSC number and liver fibrosis in a mouse model of CCl4-induced liver fibrosis. Conclusion. The hBM-MSCs act as a promising drug source against liver fibrosis development with respect to hepatopathy as a therapeutic target.

Rictor upregulation and mTORC complex 2 (mTORC2) over-activation participate in glioma cell progression, yet the underling mechanisms are not known. We here identified microRNA-153 (miR-153) as a potential anti-Rictor miRNA, which was downregulated in multiple human glioma tissues and glioma cell lines (U87MG, T98G, U373MG and U251MG). miR-153 downregulation was correlated with Rictor (mRNA and protein) upregulation and p-Akt Ser473 (the mTORC2 indicator) over-activation in the glioma tissues and cells. Our in vitro evidences suggested that Rictor could be one primary target of miR-153 in glioma cells. Exogenous overexpression of miR-153 downregulated Rictor (mRNA and protein) and decreased p-Akt Ser473 in U87MG cells, leading to significant growth inhibition and apoptosis activation. Notably, U87MG cells with Rictor shRNA knockdown showed similar phenotypes of cells with miR-153 overexpression. More importantly, in Rictor-silenced U87MG cells, miR-153 expression failed to further affect cell growth nor apoptosis. In vivo, we showed that miR-153 overexpression dramatically inhibited U87MG tumor growth in nude mice. Together, these results suggest that miR-153 downregulation could be one important reason of Rictor upregulation and mTORC2 over-activation in glioma cells. Further, miR-153-induced anti-glioma cell activity is possibly via downregulating Rictor.