Targeting pyroptosis with nanoparticles to alleviate neuroinflammatory for preventing secondary damage following traumatic brain injury.

Posttraumatic neuroinflammation is a key driver of secondary injury after traumatic brain injury (TBI). Pyroptosis, a proinflammatory form of programmed cell death, considerably activates strong neuroinflammation and amplifies the inflammatory response by releasing inflammatory contents. Therefore, treatments targeting pyroptosis may have beneficial effects on the treatment of secondary brain damage after TBI. Here, a cysteine-alanine-glutamine-lysine peptide-modified ß-lactoglobulin (ß-LG) nanoparticle was constructed to deliver disulfiram (DSF), C-ß-LG/DSF, to inhibit pyroptosis and decrease neuroinflammation, thereby preventing TBI-induced secondary injury. In the post-TBI mice model, C-ß-LG/DSF selectively targets the injured brain, increases DSF accumulation, and extends the time of the systemic circulation of DSF. C-ß-LG/DSF can alleviate brain edema and inflammatory response, inhibit secondary brain injury, promote learning, and improve memory recovery in mice after trauma. Therefore, this study likely provided a potential approach for reducing the secondary spread of TBI.

Polydopamine-based loaded temozolomide nanoparticles conjugated by peptide-1 for glioblastoma chemotherapy and photothermal therapy.

Purpose: Nanoparticles (NPs) of the polydopamine (PDA)-based,loaded with temozolomide (TMZ) and conjugated with Pep-1 (Peptide-1) as a feasible nano-drug delivery system were constructed and utilized for chemotherapy (CT) and photothermal therapy (PTT) of glioblastoma (GBM). Method: PDA NPs were synthesized from dopamine (DA) hydrochloride and reacted with TMZ to obtain the PDA-TMZ NPs and then the PDA NPs and the PDA-TMZ NPs were conjugated and modified by Pep-1 to obtain the Pep-1@PDA NPs and Pep-1@PDA-TMZ NPs via the Schiff base reaction (SBR), respectively.Their dimensions, charge, and shape were characterized by dynamic light scattering (DLS) and scanning electron microscope (SEM). The assembly of TMZ was verified by Fourier-transform infrared spectroscopy (FT-IR) and ultraviolet and visible spectroscopy (UV-Vis). The biostability of both the nanocarrier and the synthetic NPs were validated using water and fetal bovine serum (FBS). The antitumor activities of the PDA-TMZ NPs and Pep-1@PDA-TMZ NPs were verified in U87 cells and tumor-bearing nude mice. Results: The prepared PDA NPs, PDA-TMZ NPs, Pep-1@PDA NPs, and Pep-1@PDA-TMZ NPs were regular and spherical, with dimension of approximately 122, 131, 136, and 140 nm, respectively. The synthetic nanoparticles possessed good dispersity, stability,solubility, and biocompatibility. No obvious toxic side effects were observed, and the loading rate of TMZ was approximately 50%.In vitro research indicated that the inhibition ratio of the Pep-1@PDA-TMZ NPs combined with 808 nm laser was approximately 94% for U87 cells and in vivo research was approximately 77.13%, which was higher than the ratio of the other groups (p < 0.05). Conclusion: Pep-1 was conjugated and modified to PDA-TMZ NPs, which can serve as a new targeted drug nano-delivery system and can offer a CT and PTT integration therapy against GBM. Thus, Pep-1@PDA-TMZ NPs could be a feasible approach for efficient GBM therapy, and further provide some evidence and data for clinical transformation so that gradually conquer GBM.

H3F3A K27M Mutation Promotes the Infiltrative Growth of High-Grade Glioma in Adults by Activating ß-Catenin/USP1 Signaling.

H3F3A K27M (H3.3K27M) is a newly identified molecular pathological marker in glioma and is strongly correlated with the malignancy of diffuse intrinsic pontine glioma (DIPG). In recent years, accumulating evidence has revealed that other types of glioma also contain the H3.3K27M mutation. However, the role of H3.3K27M in high-grade adult glioma, the most malignant glioma, has not been investigated. In this study, we focused on exploring the expression and function of H3.3K27M in high-grade glioma in adults. We found that H3.3K27M was highly expressed at high levels in some high-grade glioma tissues. Then, we introduced H3.3K27M into H3.3 wild-type glioma cells, U87 cells and LN229 cells. We found that H3.3K27M did not affect the growth of glioma cells in vitro and in vivo; however, the survival of mice with transplanted tumors was significantly reduced. Further investigation revealed that H3.3K27M expression mainly promoted the migration and invasion of glioma cells. Moreover, we confirmed that H3.3K27M overexpression increased the levels of the ß-catenin and p-ß-catenin (Ser675) proteins, the ubiquitin-specific protease 1 (USP1) mRNA and protein levels, and the enhancer of zeste homolog 2 (EZH2) protein level. In addition, the ß-catenin inhibitor XAV-939 significantly attenuated the upregulation of the aforementioned proteins and inhibited the increased migration and invasion caused by the H3.3K27M mutation. Overall, the H3.3K27M mutation in high-grade glioma is a potential biomarker for poor prognosis mainly due to the infiltration of glioma cells that is at least partially mediated by the ß-catenin/USP1/EZH2 pathway.

ZnO Nanorods Grown on Rhombic ZnO Microrods for Enhanced Photocatalytic Activity.

In this paper, the formation of rhombic ZnO microrods surrounded by ZnO nanorods was realized on the surfaces of zinc foils using a hydrothermal method. The photocatalytic degradation of Rhodamine B solution was used to test the photocatalytic performance of the prepared samples. Compared with the rhombic Zn(OH)F and ZnO microrods grown on zinc foils, the hierarchical micro/nanostructures formed by ZnO nanorods surrounding the surfaces of rhombic ZnO microrods have better photocatalytic performance. The experimental results are mainly due to the fact that the hierarchical ZnO micro/nanostructures formed by ZnO nanorods surrounding the surface of the rhombic ZnO microrods have a larger surface area compared with the rhombic Zn(OH)F and ZnO microrods. More importantly, the photocatalytic circulation experiments indicate that ZnO nanorods grown on rhombic ZnO microrods can be recycled and have a relatively stable photocatalytic performance.

Bacteria Wear ICG Clothes for Rapid Detection of Intracranial Infection in Patients After Neurosurgery and Photothermal Antibacterial Therapy Against Streptococcus Mutans.

Bacterial infection is one of the most serious physiological conditions threatening human health. There is an increasing demand for more effective bacterial diagnosis and treatment through non-invasive approaches. Among current antibacterial strategies of non-invasive approaches, photothermal antibacterial therapy (PTAT) has pronounced advantages with properties of minor damage to normal tissue and little chance to trigger antimicrobial resistance. Therefore, we developed a fast and simple strategy that integrated the sensitive detection and photothermal therapy of bacteria by measuring adenosine triphosphate (ATP) bioluminescence following targeted photothermal lysis. First, 3-azido-d-alanine (d-AzAla) is selectively integrated into the cell walls of bacteria, photosensitizer dibenzocyclooctyne, and double sulfonic acid-modified indocyanine green (sulfo-DBCO-ICG) are subsequently designed to react with the modified bacteria through in vivo click chemistry. Next, the sulfo-DBCO-ICG modified bacteria under irradiation of 808 nm near-infrared laser was immediately detected by ATP bioluminescence following targeted photothermal lysis and even the number of bacteria on the infected tissue can be significantly reduced through PTAT. This method has demonstrated the ability to detect the presence of the bacteria for ATP value in 32 clinical samples. As a result, the ATP value over of 100 confirmed the presence of bacteria in clinical samples for 22 patients undergoing craniotomy and ten otitis media patients. Overall, this study paves a brand new avenue to facile diagnosis and a treatment platform for clinical bacterial infections.

Flexible composite film with artificial opal photonic crystals for efficient all-day passive radiative cooling.

All-day passive radiative cooling has recently attracted broader attention for its potential as a viable energy technology. Although tremendous progress has been achieved, the design and fabrication of low-cost high-efficiency radiators for all-day passive radiative cooling remains a challenge. Herein, we report a new type of flexible composite radiator film with built-in artificial opal-like structures for all-day passive radiative cooling. Using artificial opal structure concepts, the proposed polydimethylsiloxane (PDMS) radiator film with embedded polystyrene (PS) microsphere photonic crystals exhibits a sufficiently high solar reflectance of ∼92.7% when in a direct sunlight region, and a thermal emittance of ∼93.6% within the atmospheric window. Without the need for traditional reflectors like silver or aluminum foils, this composite film realizes subambient temperature reduction of ∼4.8 °C in direct sunlight and ∼8.5 °C during the night. This work provides a new fabrication approach for the low-cost production of structural polymer films for high performance and potential real word applications.

COP1 Acts as a Ubiquitin Ligase for PCDH9 Ubiquitination and Degradation in Human Glioma.

Constitutive photomorphogenic 1 (COP1, also known as RFWD2), a ring-finger-type E3 ubiquitin ligase, has been reported to play a pivotal role in the regulation of cell growth, apoptosis, and DNA repair. Accumulating evidence has suggested that COP1 plays a role in tumorigenesis by triggering the ubiquitination and degradation of its substrates, but the potential mechanism remains unclear. In this study, COP1 was used as a bait in a yeast two-hybrid experiment to screen COP1-interacting proteins in a human brain cDNA library, and the results indicated that protocadherin 9 (PCDH9) was a potential binding protein of COP1. The interaction between and colocalization of COP1 and PCDH9 was further confirmed by coimmunoprecipitation (co-IP) assay and immunofluorescent staining. Subsequently, we demonstrated that COP1 acted as an E3 ligase to promote the ubiquitination and degradation of PCDH9 through the proteasome pathway in glioma cells. Furthermore, we identified that the type of COP1 mediated PCDH9 ubiquitination was Lys48-linked polyubiquitination. Finally, we found that the COP1 protein level was inversely correlated with the PCDH9 protein level in human glioma tissues. Taken together, our results suggest that COP1 is an E3 ubiquitin ligase for PCDH9 and reveal an important mechanism for PCDH9 regulation in human glioma.

Multi-responsive nanofibers composite gel for local drug delivery to inhibit recurrence of glioma after operation.

BACKGROUND: The postoperative recurrence of malignant gliomas has presented a clinical conundrum currently. Worse, there is no standard treatment for these recurrent tumours. Therefore, novel promising methods of clinical treatment are urgently needed. METHODS: In this study, we synthesized reactive oxygen species (ROS)-triggered poly(propylene sulfide)60 (PPS60) mixed with matrix metalloproteinases (MMPs)-responsive triglycerol monostearate (T) lipids and TMZ. The mixed solution could self-assemble at 50 â„ƒ to generate hydrogels with MMPs- and ROS-responsiveness. We explored whether the T/PPS + TMZ hydrogel could achieve the MMP- and ROS-responsive delivery of TMZ and exert anti-glioma regrowth effects in vitro and in vivo. These results demonstrated that the T/PPS + TMZ hydrogel significantly improved the curative effect of TMZ to inhibit postsurgical recurrent glioma. RESULTS: The results confirmed the responsive release of TMZ encapsulated in the T/PPS + TMZ hydrogel, and the hydrogel showed excellent performance against glioma in an incomplete glioma operation model, which indicated that the T/PPS + TMZ hydrogel effectively inhibited the growth of recurrent glioma. CONCLUSION: In summary, we successfully developed injectable MMPs- and ROS-responsive hydrogels that could achieve the sustained release of TMZ in the surgical cavity to inhibit local recurrent glioma after surgery.

TSG101 Promotes the Proliferation, Migration, and Invasion of Human Glioma Cells by Regulating the AKT/GSK3ß/ß-Catenin and RhoC/Cofilin Pathways.

The tumor susceptibility gene 101 (TSG101) has been reported to play important roles in the development and progression of several human cancers, such as pancreatic cancer, prostate cancer, and hepatocellular carcinoma. However, its potential roles and underlined mechanisms in human glioma are still needed to be further clarified. This study was designed to assess the expression of TSG101 in glioma patients and its effects on glioma cell proliferation, migration, and invasion. Publicly available data revealed that TSG101 mRNA was significantly upregulated in glioma tissues, and high levels of TSG101 were associated with poor prognosis in glioma patients. Western blot and immunohistochemistry experiments further showed that the expression level of TSG101 protein was significantly upregulated in glioma patients, especially in the patients with high-grade glioma. The functional studies showed that knockdown of TSG101 suppressed the proliferation, migration, and invasion of glioma cells, while overexpression of TSG101 facilitated them. Mechanistic studies indicated that the proliferation, migration, and invasion induced by TSG101 in human glioma were related to AKT/GSK3ß/ß-catenin and RhoC/Cofilin signaling pathways. In conclusion, the above results suggest that the expression of TSG101 is elevated in glioma patients, which accelerates the proliferation, migration, and invasion of glioma cells by regulating the AKT/GSK3ß/ß-catenin and RhoC/Cofilin pathways.

Local Delivery of Minocycline and Vorinostat Targets the Tumor Microenvironment to Inhibit the Recurrence of Glioma.

BACKGROUND: Postoperative recurrence is the main reason for poor clinical outcomes in glioma patients, so preventing tumor recurrence is crucial in the management of gliomas. METHODS: In this study, the expression of matrix metalloproteinases (MMPs) in normal tissues was detected via RNA-seq analysis. Glioma cases from the public databases (The Cancer Genome Atlas (TCGA), the Chinese Glioma Genome Atlas (CGGA)) were included in this study. The hydrogel contains minocycline (Mino) and vorinostat (Vor) (G/Mino+Vor) was formed under 365 nm when the photoinitiator was added. High-performance liquid chromatography (HPLC) was used to assess the release of drugs in the G/Mino+Vor hydrogel. An MTT assay was used to explore the biosecurity of GelMA. Immunohistochemistry, ELISA, and TUNEL assays were used to demonstrate the antitumor effect of the G/Mino+Vor hydrogel. RESULTS: We successfully developed a G/Mino+Vor hydrogel. The experiments in vitro and in vivo confirmed the MMPs-responsive delivery of minocycline and vorinostat in hydrogel and the anti-glioma effect on an incomplete tumor operation model, which indicated that the G/Mino+Vor hydrogel effectively inhibited the recurrence of glioma after surgery. CONCLUSION: In summary, the G/Mino+Vor hydrogel could continuously release drugs and improve the therapy effects against recurrent glioma.

Highly linearly polarized light emission from flexible organic light-emitting devices capitalized on integrated ultrathin metal-dielectric nanograting.

Although there have been tremendous achievements ever since the first work on an organic electroluminescent (EL) device that emitted polarized light, the development of flexible polarized emission organic light-emitting devices (OLEDs) is not without hurdles, and the challenge towards real-world applications still requires tremendous effort. In this paper, we proposed highly linearly polarized light-emission from flexible green OLEDs capitalized on integrated ultrathin metal-dielectric nanograting. The acquired polarized device with meticulously optimized geometric parameters yields an angle-invariant average extinction ratio beyond 20.0 dB within a viewing angle range of ± 60°. The detailed analysis illustrates that surface plasmons and cavity modes are simultaneously contributed to the TM-polarized light selection. We hope that the presented approach will open new opportunities for designing flexible polarized light sources.

Activation of STAT1 by the FRK tyrosine kinase is associated with human glioma growth.

PURPOSE: Glioma is a highly aggressive and lethal brain tumor. Signal transducers and activators of transcription (STAT) pathway are widely implicated in glioma carcinogenesis. Our previous study found that the Fynrelated kinase (FRK) gene, plays as a tumor suppressor in the development and progression of glioma. This study aimed to investigate the role of FRK in the activation pathway of STATs and its effect on the growth of glioma. METHODS: The U251 and U87 cells with stable FRK overexpression were generated by lentivirus technique. The effects of FRK on the related proteins of STAT signaling pathway were detected by western blotting. Coimmunoprecipitation was used to detect the association of FRK and STAT1. The effects of STAT1 on the proliferation of glioma cells were detected by CCK8 or Edu cell proliferation assays. The expressions and correlation of FRK and p-STAT1 in glioma tissues were detectd by western blotting or immunohistochemistry. The effect of FRK on the growth of glioma was investigated in vivo mouse model. RESULTS: The level of p-JAK2 and p-STAT1 increased after FRK overexpression, while they decreased after FRK downregulation both in U251 and U87 cells. However, FRK had no effect on STAT3 phosphorylation. FRK-induced STAT1 activation was not dependent on JAK2. FRK associated with STAT1, induced STAT1 nuclear translocation and regulated the expressions of STAT1-related target genes. STAT1 overexpression suppressed the proliferation of glioma cells. In contrast, STAT1 knockdown by siRNA promoted glioma cell growth. Importantly, down-regulation of STAT1 partially attenuated FRK-induced growth suppression. The clinical sample-based study indicated that the expression of FRK was significantly correlated with the expression of p-STAT1. FRK significantly inhibited glioma tumor growth in vivo. CONCLUSIONS: Our findings highlighted a critical role of FRK in tumor suppression ability through promoting STAT1 activation, and provided a potential therapeutic target for glioma.

Multifunctional Silver Nanoparticle Interlayer-Modified ZnO as the Electron-Injection Layer for Efficient Inverted Organic Light-Emitting Diodes.

The insufficient electron injection constitutes the major obstacle to achieving high-performance inverted organic light-emitting diodes (OLEDs). Here, a facile electron-injection architecture featuring a silver nanoparticle (AgNPs) interlayer-modified sol-gel-derived transparent zinc oxide (ZnO) ultrathin film is proposed and demonstrated. The optimized external quantum efficiencies of the developed inverted fluorescent and phosphorescent OLEDs capitalized on our proposed electron-injection structure reached 4.0 and 21.2% at a current density of 20 mA cm-2 and increased by a factor of 1.90 and 2.86 relative to a reference device without the AgNP interlayer, while simultaneously reducing the operational voltage and substantially ameliorating the device efficiency. Detailed analyses reveal that the local surface plasmon resonance emanated from AgNPs plays three meaningful roles simultaneously: suppressing the surface plasmon polariton mode loss, aiding in energy-level alignments, and inducing and reinforcing the local exciton-plasmon coupling electric field. Among these interesting and multifunctional roles, the enhanced local exciton-plasmon coupling electric field dominates the electron injection enhancement and substantial increases the device efficiency. Additionally, the light-scattering effect also helps in recovering the trapped light energy flux and thus improves the device efficiency. The proposed approach and findings provide an alternative path to fabricate high-performance inverted OLEDs and other related organic electronic or optoelectronic devices.

Laser speckle formed disordered micro-meander structures for light extraction enhancement of flexible organic light-emitting diodes.

A new approach for efficiently recovering the wasted light energy in conventional flexible organic light-emitting diodes (FOLEDs) is developed by implementing disordered micro-meander structures (DMMs) via laser speckle holography technology. Compared to conventional flat device architecture, the structured FOLEDs with DMMs result in substantial improvement of the device efficiency and superior angular color stability. The resulting current efficiency (CE) and external quantum efficiency (EQE) are 1.31 and 1.39 times that of a common flat structure, respectively. Moreover, the proposed DMMs micro-structure simultaneously offers the unique characteristics of angular color stability with a wide viewing angle, which is usually considered as the criteria of the high-quality lighting applications. We hope that the demonstrated method could provide an alternative way for the development of high efficiency flexible OLEDs.

Synthesis of Various TiO2 Micro-/Nano-Structures and Their Photocatalytic Performance.

TiO2 micro-/nano-structures with different morphologies have been successfully synthesized via a hydrothermal method. The effects of the solvents on the morphology and structure of the obtained products have been studied. The objective of the present paper is to compare the photocatalytic properties of the obtained TiO2 products. During the synthesis process, the tetrabutyl titanate and titanium (IV) fluoride were used as the titanium source. The obtained micro-/nano-structures were characterized by field-emission scanning electron microscopy, X-ray diffraction analysis, and nitrogen adsorption-desorption isotherms. The photocatalytic activity of the samples was evaluated by the degradation of Rhodamine B solution under simulated solar irradiation. It is found that the morphologies and structures of TiO2 have a great influence on its photocatalytic activity. Compared with other samples, TiO2 flower clusters assembled with nanorods exhibited a superior photocatalytic activity in the degradation of Rhodamine B.

PHAP1 promotes glioma cell proliferation by regulating the Akt/p27/stathmin pathway.

PHAP1 (Putative HLA-DR-associated protein 1), also termed acidic leucine-rich nuclear phosphoprotein 32A (ANP32A), Phosphoprotein 32 (pp32) or protein phosphatase 2A inhibitor (I1PP2A), is a multifunctional protein aberrantly expressed in multiple types of human cancers. However, its expression pattern and clinical relevance in human glioma remain unknown. In this study, Western blotting and immunohistochemistry analysis demonstrated PHAP1 protein was highly expressed in glioma patients, especially in those with high-grade disease. Publicly available data also revealed high levels of PHAP1 were associated with poor prognosis in glioma patients. The functional studies showed that knock-down of PHAP1 suppressed the proliferation of glioma cells, while overexpression of PHAP1 facilitated it. The iTRAQ proteomic analysis suggested that stathmin might be a potential downstream target of PHAP1. Consistently, PHAP1 knock-down significantly decreased the expression of stathmin, while overexpression of PHAP1 increased it. Also, the upstream negative regulator, p27, expression levels increased upon PHAP1 knock-down and decreased when PHAP1 was overexpressed. As a result, the phosphorylated Akt (S473), an upstream regulator of p27, expression levels decreased upon silencing of PHAP1, but elevated after PHAP1 overexpression. Importantly, we demonstrate the p27 down-regulation, stathmin up-regulation and cell proliferation acceleration induced by PHAP1 overexpression were dependent on Akt activation. In conclusion, the above results suggest that PHAP1 expression is elevated in glioma patients, which may accelerate the proliferation of glioma cells by regulating the Akt/p27/stathmin pathway.

A facile and green approach to prepare carbon dots with pH-dependent fluorescence for patterning and bioimaging.

As the new representative in the carbonaceous family, carbon dots (CDs) have gained remarkable research interests over the past decade. Herein, we report the facile preparation and thorough performance comparison of three types of carbon dots with the adoption of ubiquitous natural fruit juice as precursors and demonstrate their application in pH sensing, patterning and bioimaging. All the yielded CDs show interesting optical properties including evident single- or two-photon absorption and excitation-dependent photoluminescence along with the high fluorescent yield. A detailed study on the physical properties by EPR and Stokes shift analysis and structural composition analysis by XPS and Raman spectroscopy suggest that the fluorescence of CDs originates from the electron-hole recombination via the defect state. In addition, through the regulation of non-radiative recombination rate of CDs, all the obtained CDs could be applied as fluorescent sensing platforms toward the sensitive detection of the solution pH changes by the indication of CDs' fluorescent yield and lifetime variation. Moreover, it was also proven that the resulting CDs could be employed as fluorescent inks for printing patterns in anti-counterfeit applications and as fluorescent probes for bioimaging of osteoblasts.

Loss of SH3GL2 promotes the migration and invasion behaviours of glioblastoma cells through activating the STAT3/MMP2 signalling.

SH3GL2 (Src homology 3 (SH3) domain GRB2-like 2) is mainly expressed in the central nervous system and regarded as a tumour suppressor in human glioma. However, the molecular mechanism of the SH3GL2 protein involved in malignant behaviours of human glioma has not been elucidated. In this study, we tried to investigate the role of SH3GL2 in glioma cell migration and invasion and explore its underlined molecular mechanism. Firstly, we discovered that the protein level of SH3GL2 was widely decreased in the human glioma patients, especially in high-grade glioma tissues. Then, we determined the role of SH3GL2 in migration and invasion of glioma cells upon SH3GL2 knocking down and overexpressing. It was showed that knocking down of SH3GL2 promoted the migration and invasion of glioma cells, whereas overexpression of SH3GL2 inhibited them. Further study on molecular mechanism disclosed that silencing of SH3GL2 obviously activated the STAT3 (signal transducer and activator of transcription 3) signalling thereby promoting the expression and secretion of MMP2. On the contrary, overexpression of SH3GL2 had opposite effect. Taken together, the above results suggest that SH3GL2 suppresses migration and invasion behaviours of glioma cells through negatively regulating STAT3/MMP2 signalling and that loss of SH3GL2 may intensify the STAT3/MMP2 signalling thereby contributing to the migration and invasion of glioma cells.

Jab1 promotes glioma cell proliferation by regulating Siah1/ß-catenin pathway.

Jab1 (Jun activation domain-binding protein 1), also known as CSN5 (COP9 signalosome subunit 5), is frequently overexpressed in several cancer types. However, the biological functions and the molecular mechanisms of the Jab1 protein in human gliomas have not been investigated. In this study, we found that Jab1 protein was increasingly expressed in human glioma tissues comparing with normal brain tissues (Non-tumor). This suggested that Jab1 might be involved in the development of glioma. Thus, the role of Jab1 in glioma cell proliferation was investigated using Jab1 loss- and gain-of-function. The results showed that downregulation of Jab1 significantly inhibited glioma cell proliferation, while overexpression of Jab1 promoted it. Further investigation on molecular targets revealed that silencing of Jab1 obviously increased the p53 protein level thereby promoting the transcription of ubiquitin ligase Siah1 (Seven in absentia homolog 1), which aggravates the degradation of ß-catenin. In contrast, overexpression of Jab1 had the opposite effect. Taken together, these findings suggest that Jab1 promotes glioma cell proliferation and increased expression of Jab1 in glioma patients may amplify ß-catenin signaling to contribute to glioma cell proliferation.