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AimsCyclooxygenase-2 (COX-2)/soluble epoxide hydrolase (sEH) dual inhibitor, PTUPB, has been demonstrated to inhibit angiogenesis, primary tumor growth and metastasis. The aim of this study is to investigate the effects of PTUPB on glioblastoma cells and xenograft model.ResultsWe show here that PTUPB inhibits glioblastoma cell proliferation and G1 phase cell cycle arrest in vitro, and suppresses the tumor growth and angiogenesis in vivo. The expression and activation of epidermal growth factor receptor (EGFR) and its downstream kinases, ERK1/2 and AKT, are reduced by PTUPB, indicating that the EGF/EGFR signaling pathway is a potential target. Moreover, PTUPB dramatically suppresses expression of hyaluronan mediated motility receptor (HMMR) in the glioblastoma cell lines and xenograft mouse model, suggesting that the HMMR is the other potential target.Materials and methodsCellular immunofluorescence assays were used for cell staining of actin fibers and HMMR. CCK-8 kit was used for cell proliferation assay. Cell-cycle analysis was performed by flow cytometry. Quantitative real-time PCR assay was performed to test mRNA level. Western blot analysis was used to test protein expression. Immunohistochemical staining assay was used for xenograft tumor tissue staining of Ki-67, CD31 and HMMR. The SPSS version 17.0 software was applied for statistical analysis.ConclusionsOur data demonstrate that PTUPB is a potential therapeutic agent to treat glioblastomas.

AbstractA physical model of soft tissue that provides realistic and real-time haptic and visual feedback is crucial for neurosurgical procedures. This paper investigates the interaction between surgical instruments and soft brain tissue, proposing a soft tissue deformation simulation method based on the principle of energy minimization and constrained energy function. The model includes a permanent deformation energy function induced by friction and a volume preservation energy function to more accurately depict tissue response during procedures such as resection of convex meningiomas and evacuation of intracerebral hematomas. Experimental results show that the proposed method meets the requirements of neurosurgical simulation. [ABSTRACT FROM AUTHOR]

Purpose: Anlotinib is a multi-target TKI which has been used in different advanced tumors. However, its efficiency and safety in patients with glioblastoma are still not well discussed. This retrospective study aimed to discover the safety and efficiency of anlotinib in recurrent grade 4 glioma., Methods: The clinical data of patients with recurrent grade 4 glioma treated with anlotinib in our center were collected and analyzed. The progression-free survival (PFS), overall survival (OS), and OS after recurrence were calculated by Kaplan-Meier method and compared by log-rank test. Sub-group analysis was used to find possible variables that affect survival., Results: From October 2017 to December 2020, seventeen patients with recurrent grade 4 glioma treated with anlotinib were enrolled. The median age was 50 with 13 males. The median KPS was 70. All patients received standard STUPP mode treatment before recurrence. The median PFS was 7 months [95% confidence interval (CI) 5.3-8.6]. The median OS after first diagnosis was 17 months (95% CI 15.7-18.3). The median OS after recurrence was 10 months (95% CI 7.6-12.4). The objective response rate was 33.33% (5/15), and the disease control rate was 60% (9/15). The existence of target genes was identified as a variable affecting the survival after recurrence. The median OS after recurrence in patients with target genes was 12 months (95% CI 6.9-17.1), whereas for patients without targets, the median OS was 4 months (95% CI 1.9-6.1) and for patients with an unknown status, the median OS was 10 months (95% CI 8.4-11.6) (P = 0.013)., Conclusion: For recurrent grade 4 glioma, anlotinib can be considered as a supplement to the standard STUPP treatment, especially for the patient with anlotinib target genes., (Copyright © 2024 Copyright: © 2024 Neurology India, Neurological Society of India.)

Krüppel-like factor 2 (KLF2) is a member of the zinc finger family, which is considered a potential tumor suppressor gene due to its reduced expression in gastric cancer. MicroRNAs (miRNAs) are a class of short non-coding single-stranded RNAs that are closely related to the development of gastric cancer. The purpose of this study was to investigate the miRNAs that regulate KLF2 and explore its specific mechanism in gastric cancer. Bioinformatics software Targetscan identified that microRNA-32-5p (miRNA-32-5p) may bind to KLF2 mRNA to regulate its expression. In order to verify the regulatory effect of miRNA-32-5p on KLF2, the proliferation and migration assays were performed in both KLF2 overexpression and KLF2 knockdown gastric cancer cells. Dual-Luciferase reporter assay proved that KLF2 could bind to the PTEN promoter to induce its expression. Moreover, research on molecular mechanisms indicated that both miRNA-32-5p and shKLF2 downregulated the expression of PTEN and activated the PI3K/AKT signaling to promote the development of gastric cancer. Targeting miRNA-32-5p and KLF2 is expected to provide new sign and target for gastric cancer treatment., Competing Interests: None.

Glioblastoma multiforme (GBM), the most commonly occurring primary intracranial tumor, is associated with a negative outcome, regardless of the availability of multimodal therapies. However, the identification of glioma stem cells (GSCs), which are small groups of cells within the GBM, has resulted in novel avenues for research. GSCs are resistant to numerous types of environmental stress, such as irradiation, antitumor drugs and hypoxia. Nuclear factor erythroid 2-related factor 2 (Nrf2) has a significant role the cellular response to oxidative stress and previous studies have supported the significance of Nrf2 in GBM; however, the role of Nrf2 in GSCs remains unclear. In the present study, Nrf2 in CD133 - GBM cells and CD133 + GSCs from GBM were compared. GSCs from GBM, which express the surface marker CD133, were separated by magnetic cell sorting and analyzed by immunofluorescence in 24-well clusters and cell counting using flow cytometry. The expression of Nrf2 was detected at the transcriptional and translational levels in CD133 + and CD133 - cells, and the result indicated that GSCs were successfully isolated from the GBM. The percentage of tumor stem cells in total cells was between 0.49 and 0.91%. Nrf2 was overexpressed in CD133 + GSCs when compared with CD133 - GBM cells, which indicated that the expression of Nrf2 in GSCs was closely correlated with malignant proliferation and differentiation of the GBM. Therefore, it was concluded that Nrf2 may be a potential biomarker and rational therapeutic target in GBM.