a-modified-mouse-model-intracranial-aneurysm-based-on-hemodynamic

A Modified Mouse Model of Intracranial Aneurysm Based on Hemodynamic Change and Hypertension

Intracranial aneurysm (IA) poses a significant health risk due to morbidity and mortality associated with aneurysm rupture. However, the molecular ...

the Affiliated Hospital of Guizhou Medical University

The authors report a case of a woman aged 33 years who suffered from the combination of primary gliosarcoma and arteriovenous malformation as the first clinical presentation of intracranial hemorrhage.

The Coexistence of Gliosarcoma and Arteriovenous Malformation with the BRAF V600E Mutation.

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. Additionally, the U87MG and U251 cell lines showed low levels of EphB3 expression. This finding was consistent with the negative correlation between EphB3 expression in glioma tissues and tumor grade. Depletion of EphB3 gene in U87MG and U251 cell lines resulted in a substantial enhancement of their invasion, migration, and proliferation capacities in vitro. Furthermore, the knockdown of EphB3 led to an upregulation of EGFR, p-PI3K, and p-AKT protein levels. On the other hand, EphB3 overexpression reduced the invasiveness, proliferative capacity and migration rate of U87MG and U251 cells, and downregulated EGFR, p-PI3K and p-AKT. These findings indicate that EphB3 functions as a tumor suppressor in glioma, and its downregulation enhances the malignant potential of glioma cells by activating the EGFR-PI3K/AKT pathway. Thus, EphB3 is a promising diagnostic marker for glioma, and the EphB3-EGFR-PI3K / AKT axis deserves further investigation as a potential therapeutic target.

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

In recent years, abnormal expression of collagen triple helix repeat containing 1 (CTHRC1) has been found in some tumors, closely related to the poor prognosis of cancer patients. However, the clinical significance of CTHRC1 in gliomas is not completely understood.

Expression, Prognostic Value, and Biological Function of CTHRC1 in Different Types of Gliomas: A Bioinformatic Analysis and Experiment Validation.

To explore the efficacy of a prediction model based on diffusion-weighted imaging (DWI) features extracted from deep learning (DL) and radiomics combined with clinical parameters and apparent diffusion coefficient (ADC) values to identify microsatellite instability (MSI) in endometrial cancer (EC).

A prediction model based on deep learning and radiomics features of DWI for the assessment of microsatellite instability in endometrial cancer.

Recent research has found that ferroptosis is the most prevalent type of programmed cell death in glioma tissues and is associated with malignant progression, poor prognosis, and exacerbated immune suppression in glioblastoma (GBM). In recent years, nuclear receptor coactivator 4 (NCOA4) has been identified as a key protein in ferroptosis, but its expression in GBM tissues remains unclear. We observed an intriguing phenomenon where the expression pattern of NCOA4 was opposite in GBM tissues compared to three GBM cell lines (U87-MG, U251, and LN229), with NCOA4 expression being elevated in brain tissue but decreased in the GBM cells. This observation was further confirmed through bioinformatics analysis and experiments. Based on this finding, we hypothesize that immune cells in GBM tissues may exhibit more pronounced signs of iron depletion compared to tumor cells, which could contribute to the therapeutic resistance of GBM. The increase in NCOA4 observed in tumor tissues does not necessarily reflect increased ferroptosis in tumor cells but might indicate increased ferroptosis in non-tumor cells. This point should be considered when evaluating the efficacy of inducing ferroptosis via NCOA4 in GBM research. This observation could potentially impact the proposed strategy of inducing iron depletion as a treatment for GBM. We recognize the importance of this finding for guiding future GBM research and believe it warrants further investigation. This phenomenon may also be present in other types of tumors.

Opposite expression of NCOA4 in glioblastoma tissues and cell lines.

Low-grade glioma (LGG) is a primary brain tumor with relatively low malignancy. NCOA4 is a key regulator of ferritinophagy-related processes and is involved in the occurrence and development of many cancers. However, the role of NCOA4 in LGG remains poorly understood.

Article	Year
The Coexistence of Gliosarcoma and Arteriovenous Malformation with the BRAF V600E Mutation. World neurosurgery\| PubMed ID: 31759151	2020
EphB3 receptor suppressor invasion, migration and proliferation in glioma by inhibiting EGFR-PI3K/AKT signaling pathway. Brain research\| PubMed ID: 38341169	2024
Expression, Prognostic Value, and Biological Function of CTHRC1 in Different Types of Gliomas: A Bioinformatic Analysis and Experiment Validation. Clinical Medicine Insights. Oncology\| PubMed ID: 38894702	2024
A prediction model based on deep learning and radiomics features of DWI for the assessment of microsatellite instability in endometrial cancer. Cancer medicine\| PubMed ID: 39171859	2024
Opposite expression of NCOA4 in glioblastoma tissues and cell lines. International immunopharmacology\| PubMed ID: 39383786	2024
Expression and prognostic value of ferritinophagy-related NCOA4 gene in low-grade glioma: integration of bioinformatics and experimental validation. BMC neurology\| PubMed ID: 39825225	2025

Xi Zeng

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