Dose-dependent developmental fluoride exposure leads to neurotoxicity and impairs excitatory synapse development.

Developmental fluoride exposure has been implicated in cognitive deficits and neurotoxicity, yet the mechanisms underlying these effects remain unclear. Here, we investigated the dose- and time-dependent impacts of sodium fluoride (NaF) on neuronal morphology, viability, oxidative stress, and synaptic function using both in vitro and in vivo mouse models. Cultured primary embryonic mouse cortical neurons were exposed to varying concentrations of NaF (0-200 μg/ml).

ATXN3 deubiquitinates ZEB1 and facilitates epithelial-mesenchymal transition in glioblastoma.

The activation of epithelial-mesenchymal transition (EMT) promotes glioblastoma (GBM) invasion, thereby enhancing its malignancy. Elucidating the underlying mechanisms that regulate EMT is essential for the development of effective treatments for GBM. In this study, we found that GBM tissues and cells exhibit significantly elevated expression levels of ataxin 3 (ATXN3).

Inhibition of Bruton's tyrosine kinase restricts neuroinflammation following intracerebral hemorrhage.

Intracerebral hemorrhage (ICH) is a devastating form of stroke with a lack of effective treatments. Following disease onset, ICH activates microglia and recruits peripheral leukocytes into the perihematomal region to amplify neural injury. Bruton's tyrosine kinase (BTK) controls the proliferation and survival of various myeloid cells and lymphocytes.

CD22 blockade exacerbates neuroinflammation in Neuromyelitis optica spectrum disorder.

Background: Neuromyelitis optica spectrum disorder (NMOSD) is an autoantibody-triggered central nervous system (CNS) demyelinating disease that primarily affects the spinal cord, optic nerves and brainstem. Among the first responders to CNS injury, microglia are prominent players that drive NMOSD lesion formation. However, the key molecular switches controlling the detrimental activity of microglia in NMOSD are poorly understood.

Combined simultaneous transsphenoidal and transcranial regimen improves surgical outcomes in complex giant pituitary adenomas: a longitudinal retrospective cohort study.

Background: Surgical treatment of complex giant pituitary adenomas (GPAs) presents significant challenges. The efficacy and safety of combining transsphenoidal and transcranial approaches for these tumors remain controversial. In this largest cohort of patients with complex GPAs, we compared the surgical outcomes between those undergoing a combined regimen and a non-combined regimen.

EphB3 receptor suppressor invasion, migration and proliferation in glioma by inhibiting EGFR-PI3K/AKT signaling pathway.

Eph receptors are the largest subfamily of receptor tyrosine kinases, and they have been shown to play a crucial role in glioma. The EphB3 receptor is a member of this family, and its effect on the invasion, migration and proliferation of glioma cells was examined in this study. It was found that the expression of EphB3 was decreased in glioma specimens with increasing tumor grade.

The role of tumor-associated macrophages in glioma cohort: through both traditional RNA sequencing and single cell RNA sequencing.

Gliomas are the leading cause in more than 50% of malignant brain tumor cases. Prognoses, recurrences, and mortality are usually poor for gliomas that have malignant features. In gliomas, there are four grades, with grade IV gliomas known as glioblastomas (GBM).

USP10 deubiquitinates RUNX1 and promotes proneural-to-mesenchymal transition in glioblastoma.

The mesenchymal (MES) subtype of glioblastoma (GBM) is a highly aggressive, malignant and proliferative cancer that is resistant to chemotherapy. Runt-related transcription factor 1 (RUNX1) was shown to support MES GBM, however, its underlying mechanisms are unclear. Here, we identified USP10 as a deubiquitinating enzyme that regulates RUNX1 stabilization and is mainly expressed in MES GBM.

PRL1 Promotes Glioblastoma Invasion and Tumorigenesis Activating USP36-Mediated Snail2 Deubiquitination.

Regenerating liver phosphatase 1 (PRL1) is an established oncogene in various cancers, although its biological function and the underlying mechanisms in glioblastoma multiforme (GBM) remain unclear. Here, we showed that PRL1 was significantly upregulated in glioma tissues and cell lines, and positively correlated with the tumor grade. Consistently, ectopic expression of PRL1 in glioma cell lines significantly enhanced their tumorigenicity and invasion both and by promoting epithelial-mesenchymal transition (EMT).

A Candidate Prognostic Biomarker Complement Factor I Promotes Malignant Progression in Glioma.

Glioma is the most common and aggressive type of primary central nervous system (CNS) tumor in adults and is associated with substantial mortality rates. The aim of our study was to evaluate the prognostic significance and function of the complement factor I (CFI) in glioma. The expression levels of CFI in glioma tissues and the survival of the CFI and CFI patient groups were analyzed using The Cancer Genome Atlas (TCGA) database and Genotype-Tissue Expression (GTEx).

USP18 deubiquitinates and stabilizes Twist1 to promote epithelial-mesenchymal transition in glioblastoma cells.

Aberrant activation of epithelial-mesenchymal transition (EMT) pathway drives the invasion and migration of multiple cancers including glioblastoma (GBM). Clinical interventions focused on inhibiting EMT are of increasing interest in the treatment of GBM. In the present study, we discovered that glioma tissues and cells, especially GBMs show significantly up-modulated ubiquitin-specific protease 18 (USP18) expression.

Hypoxia-induced EPHB2 promotes invasive potential of glioblastoma.

EphB2, a receptor tyrosine kinase for ephrin ligands, is overexpressed in various cancers and plays an important role in tumor progression. EPHB2 promotes endothelial-mesenchymal transition (EMT) and elicits associated pathologic characteristics of glioblastoma multiforme (GBM) such as invasion and migration. However, the mechanisms of the EPHB2 regulatory network in glioma remain enigmatic.

MicroRNA-1231 exerts a tumor suppressor role through regulating the EGFR/PI3K/AKT axis in glioma.

Purpose: MicroRNAs (miRNAs) have been shown to be involved in the initiation and progression of glioma. However, the underlying molecular mechanisms are still unclear.

Methods: We performed microarray analysis to evaluate miRNA expression levels in 158 glioma tissue samples, and examined miR-1231 levels in glioma samples and healthy brain tissues using qRT-PCR.

MicroRNA-625 inhibits the proliferation and increases the chemosensitivity of glioma by directly targeting AKT2.

Glioma is a malignant tumor for which new therapies are needed. Growing evidence has demonstrated that microRNAs (miRNAs) have a major effect on glioma development. Here, we aimed to characterize a novel anti-cancer miRNA, miR-625, by investigating its expression, function, and mechanism of action in glioma progression.

The Error-Prone DNA Polymerase κ Promotes Temozolomide Resistance in Glioblastoma through Rad17-Dependent Activation of ATR-Chk1 Signaling.

The acquisition of drug resistance is a persistent clinical problem limiting the successful treatment of human cancers, including glioblastoma (GBM). However, the molecular mechanisms by which initially chemoresponsive tumors develop therapeutic resistance remain poorly understood. In this study, we report that Pol κ, an error-prone polymerase that participates in translesion DNA synthesis, was significantly upregulated in GBM cell lines and tumor tissues following temozolomide treatment.

c-Myc-miR-29c-REV3L signalling pathway drives the acquisition of temozolomide resistance in glioblastoma.

Resistance to temozolomide poses a major clinical challenge in glioblastoma multiforme treatment, and the mechanisms underlying the development of temozolomide resistance remain poorly understood. Enhanced DNA repair and mutagenesis can allow tumour cells to survive, contributing to resistance and tumour recurrence. Here, using recurrent temozolomide-refractory glioblastoma specimens, temozolomide-resistant cells, and resistant-xenograft models, we report that loss of miR-29c via c-Myc drives the acquisition of temozolomide resistance through enhancement of REV3L-mediated DNA repair and mutagenesis in glioblastoma.