Chondroblastoma of the occipital bone with aneurysmal bone cyst: A rare case report.

BACKGROUND: Chondroblastoma is a rare, benign bone tumor originating from immature chondrocytes, typically found in the epiphyseal plates of long bones. Its occurrence in the skull, particularly the occipital bone, is extremely rare. CASE PRESENTATION: We report a 10-year-old girl presenting with paroxysmal dizziness, occipital pain, and a palpable mass. Imaging studies revealed an osteolytic lesion in the occipital bone with a multiloculated appearance, indicating a concomitant aneurysmal bone cyst. The patient underwent craniotomy with complete tumor excision. Postoperative follow-up showed no neurological deficits or complications and MRI confirmed no recurrence. CONCLUSION: This case highlights the rare presentation of occipital bone chondroblastoma and emphasizes the importance of early surgical intervention for positive outcomes in pediatric patients.

A pan-cancer analysis of the oncogenic role of ATP binding cassette subfamily E member 1 (ABCE1) in human tumors: An observational study.

ATP-binding-cassette subfamily E member 1 (ABCE1) has been identified as an essential component of RNA translation and cell proliferation. However, studies on its role in pan-cancer are limited. Here, we aimed to characterize ABCE1 expression and its potential biological functions in cancer. ABCE1 expression was analyzed using RNA-seq data from The Cancer Genome Atlas (TCGA), the Genotype-Tissue Expression (GTEx) database, and the Clinical Proteomic Tumor Analysis Consortium database. The prognostic value of ABCE1 was analyzed using clinical survival data from TCGA. We downloaded the immune cell infiltration score of TCGA samples from published articles and online databases and performed a correlation analysis between immune cell infiltration levels, chemokines/chemokine receptors, and ABCE1 expression. We further assessed the association between ABCE1-correlated genes and their functions in pancreatic adenocarcinoma (PAAD). In general, ABCE1 gene expression was upregulated in most tumors. There were significant strong correlations between ABCE1 expression and tumor-infiltrating cells in cancers. Furthermore, RNA transport and ribosome biogenesis were significantly related to ABCE1 expression in PAAD. Our study revealed that ABCE1 may serve as a potential prognostic and immunological pan-cancer biomarker. Moreover, ABCE1 may be used in the development of a novel target for PAAD.

Kaiso (ZBTB33) Downregulation by Mirna-181a Inhibits Cell Proliferation, Invasion, and the Epithelial-Mesenchymal Transition in Glioma Cells.

BACKGROUND/AIMS: Kaiso (ZBTB33) expression is closely associated with the progression of many cancers and microRNA (miRNA) processing. MiR-181a plays critical roles in multiple cancers; however, its precise mechanisms in glioma have not been well clarified. The goal of this study was to evaluate the interaction between Kaiso and miR-181a in glioma. METHODS: Quantitative real-time PCR (qRT-PCR) was performed to detect the levels of Kaiso and miR-181a in glioma tissues and cell lines. Cell proliferation, invasion, and the epithelial-mesenchymal transition (EMT) were evaluated to analyze the biological functions of miR-181a and Kaiso in glioma cells. The mRNA and protein levels of Kaiso were measured by qRT-PCR and western blotting, respectively. Meanwhile, luciferase assays were performed to validate Kaiso as a miR-181a target in glioma cells. RESULTS: We found that the level of miR-181a was the lowest among miR-181a-d in glioma tissues and cell lines, and the low level of miR-181a was closely associated with the increased expression of Kaiso in glioma tissues. Moreover, transfection of miR-181a significantly inhibited the proliferation, invasion, and EMT of glioma cells, whereas knockdown of miR-181a had the opposite effect. Bioinformatics analysis predicted that Kaiso was a potential target gene of miR-181a, and the luciferase reporter assay demonstrated that miR-181a could directly target Kaiso. In addition, Kaiso silencing had similar effects as miR-181a overexpression in glioma cells, whereas overexpression of Kaiso in glioma cells partially reversed the inhibitory effects of the miR-181a mimic. Conclusionss: miR-181a inhibited the proliferation, invasion, and EMT of glioma cells by directly targeting and downregulating Kaiso expression.

Oxymatrine induces cell cycle arrest and apoptosis and suppresses the invasion of human glioblastoma cells through the EGFR/PI3K/Akt/mTOR signaling pathway and STAT3.

Oxymatrine (OM), a natural quinolizidine alkaloid extracted from the traditional Chinese herb Sophora flavescens, has been revealed to produce antitumor activities in various cancer cell lines, including glioblastoma lines, in vitro. However, the mechanisms by which OM exerts its antitumor effect against glioma are poorly understood. The aim of this study was to investigate the role of OM in the proliferation, apoptosis and invasion of glioma cells and to reveal the underlying mechanisms. The effects of OM on U251MG cells in vitro were determined using a Cell Counting Kit­8 (CCK­8) assay, flow cytometric analysis, Annexin V­FITC/PI staining, DAPI staining, a terminal deoxynucleotidyl transferase­mediated dUTP nick end­labeling (TUNEL) assay, a Transwell assay and western blotting. Our data indicated that OM inhibited proliferation, arrested the cell cycle at the G0/G1 phase, decreased the expression levels of G1 cell cycle regulatory proteins (cyclin D1, CDK4 and CDK6), inhibited invasion and induced apoptosis in glioma cells. Additional investigations revealed that the expression levels of p­STAT3 and key proteins in the EGFR/PI3K/Akt/mTOR signaling pathway, such as p­EGFR, p­Akt and p­mTOR, were markedly decreased after OM treatment, while the total STAT3, EGFR, Akt and mTOR levels were not affected. These findings indicated that the EGFR/PI3K/Akt/mTOR signaling pathway and STAT3 suppression may be a potential mechanism of the OM­mediated antitumor effect in glioblastoma cells and that EGFR may be a target of OM. Hence, OM may be a promising drug and may offer a novel therapeutic strategy for malignant gliomas in the future.

Arsenic trioxide induces apoptosis and the formation of reactive oxygen species in rat glioma cells.

BACKGROUND: Arsenic trioxide (As2O3) has a dramatic therapeutic effect on acute promyelocytic leukemia (APL) patients. It can also cause apoptosis in various tumor cells. This study investigated whether As2O3 has an antitumor effect on glioma and explored the underlying mechanism. RESULTS: MTT and trypan blue assays showed that As2O3 remarkably inhibited growth of C6 and 9 L glioma cells. Cell viability decreased in glioma cells to a greater extent than in normal glia cells. The annexin V-FITC/PI and Hoechest/PI staining assays revealed a significant increase in apoptosis that correlated with the duration of As2O3 treatment and occurred in glioma cells to a greater extent than in normal glial cells. As2O3 treatment induced reactive oxygen species (ROS) production in C6 and 9 L cells in a time-dependent manner. Cells pretreated with the antioxidant N-acetylcysteine (NAC) showed significantly lower As2O3-induced ROS generation. As2O3 significantly inhibited the expression of the anti-apoptotic gene Bcl-2, and upregulated the proapoptotic gene Bax in both C6 and 9 L glioma cells in a time-dependent manner. CONCLUSIONS: As2O3 can significantly inhibit the growth of glioma cells and it can induce cell apoptosis in a time- and concentration-dependent manner. ROS were found to be responsible for apoptosis in glioma cells induced by As2O3. These results suggest As2O3 is a promising agent for the treatment of glioma.

Lack of mitochondrial ferritin aggravated neurological deficits via enhancing oxidative stress in a traumatic brain injury murine model.

Oxidative stress has been strongly implicated in the pathogenesis of traumatic brain injury (TBI). Mitochondrial ferritin (Ftmt) is reported to be closely related to oxidative stress. However, whether Ftmt is involved in TBI-induced oxidative stress and neurological deficits remains unknown. In the present study, the controlled cortical impact model was established in wild-type and Ftmt knockout mice as a TBI model. The Ftmt expression, oxidative stress, neurological deficits, and brain injury were measured. We found that Ftmt expression was gradually decreased from 3 to 14 days post-TBI, while oxidative stress was gradually increased, as evidenced by reduced GSH and superoxide dismutase levels and elevated malondialdehyde and nitric oxide levels. Interestingly, the extent of reduced Ftmt expression in the brain was linearly correlated with oxidative stress. Knockout of Ftmt significantly exacerbated TBI-induced oxidative stress, intracerebral hemorrhage, brain infarction, edema, neurological severity score, memory impairment, and neurological deficits. However, all these effects in Ftmt knockout mice were markedly mitigated by pharmacological inhibition of oxidative stress using an antioxidant, N-acetylcysteine. Taken together, these results reveal an important correlation between Ftmt and oxidative stress after TBI. Ftmt deficiency aggravates TBI-induced brain injuries and neurological deficits, which at least partially through increasing oxidative stress levels. Our data suggest that Ftmt may be a promising molecular target for the treatment of TBI.

A test of climate, sun, and culture relationships from an 1810-year Chinese cave record.

A record from Wanxiang Cave, China, characterizes Asian Monsoon (AM) history over the past 1810 years. The summer monsoon correlates with solar variability, Northern Hemisphere and Chinese temperature, Alpine glacial retreat, and Chinese cultural changes. It was generally strong during Europe's Medieval Warm Period and weak during Europe's Little Ice Age, as well as during the final decades of the Tang, Yuan, and Ming Dynasties, all times that were characterized by popular unrest. It was strong during the first several decades of the Northern Song Dynasty, a period of increased rice cultivation and dramatic population increase. The sign of the correlation between the AM and temperature switches around 1960, suggesting that anthropogenic forcing superseded natural forcing as the major driver of AM changes in the late 20th century.