Targeted Pyroptosis with Resveratrol Nanoparticles to Reduce Secondary Brain Injury and Post-Traumatic Epilepsy.

Traumatic brain injury (TBI) is associated with high mortality and disability rates globally, leading to significant sequelae, particularly post-traumatic epilepsy (PTE), which severely impacts physical health and quality of life. TBI involves primary and secondary damage, with the latter exacerbating the initial injury through neuroinflammation, influencing the overall outcome. Recent studies highlight pyroptosis as a crucial factor in the spread of secondary brain damage and the development of epilepsy, making it a vital therapeutic target.

MEX3A Impairs DNA Mismatch Repair Signaling and Mediates Acquired Temozolomide Resistance in Glioblastoma.

Unlabelled: MutS protein homolog 2 (MSH2) is a key element involved in the DNA mismatch repair (MMR) system, which is responsible for recognizing and repairing mispaired bases. Simultaneously, MSH2 identifies DNA adducts induced by temozolomide (TMZ) and triggers apoptosis and autophagy in tumor cells. Previous work has revealed that reduced MSH2 expression is often observed in patients with glioblastoma (GBM) who relapse after chemotherapy.

Efficient Dye Contaminant Elimination and Simultaneously Electricity Production via a Bi-Doped TiO Photocatalytic Fuel Cell.

TiO develops a higher efficiency when doping Bi into it by increasing the visible light absorption and inhibiting the recombination of photogenerated charges. Herein, a highly efficient Bi doped TiO photoanode was fabricated via a one-step modified sol-gel method and a screen-printing technique for the anode of photocatalytic fuel cell (PFC). A maximum degradation rate of 91.

Imipramine impedes glioma progression by inhibiting YAP as a Hippo pathway independent manner and synergizes with temozolomide.

Patients with malignant glioma often suffered from depression, which leads to an increased risk of detrimental outcomes. Imipramine, an FDA-approved tricyclic antidepressant, has been commonly used to relieve depressive symptoms in the clinic. Recently, imipramine has been reported to participate in the suppression of tumour progression in several human cancers, including prostate cancer, colon cancer and lymphomas.

TGF-β1 modulates temozolomide resistance in glioblastoma via altered microRNA processing and elevated MGMT.

Background: Our previous studies have indicated that miR-198 reduces cellular methylguanine DNA methyltransferase (MGMT) levels to enhance temozolomide sensitivity. Transforming growth factor beta 1 (TGF-β1) switches off miR-198 expression by repressing K-homology splicing regulatory protein (KSRP) expression in epidermal keratinocytes. However, the underlying role of TGF-β1 in temozolomide resistance has remained unknown.

Effects of Long Form of CAPON Overexpression on Glioma Cell Proliferation are Dependent on AKT/mTOR/P53 Signaling.

CAPON has two isoforms in human brain: long form of CAPON (CAPON-L) and short form of CAPON (CAPON-S). Recent studies have indicated the involvement of CAPON in tumor cell growth. We aimed to reveal the role of the two CAPON isoforms in the proliferation of glioma cells in this study.

Transparent conductive film based on silver nanowires and single-wall carbon nanotubes for transparent heating films.

In this paper, hybrid transparent conductive films (TCFs) are designed by combining silver nanowires with the single-wall carbon nanotubes (SWCNTs) and the transparent heating films (THFs) based on the TCFs are evaluated for possible vehicle applications. By comparing the properties, including the transmittance, sheet resistance, microstructure and heating curves, we found that the SWCNTs/AgNWs are considerably suitable for making THFs. The after-treatment methods, such as physical method (hot roll pressing) and chemical method (nitric acid and Poly (diallydimethylammonium chloride) solution, (PDAC)) were researched in detail to optimize the sheet resistance and transparency to fit the THF requirements.

Fstl1/DIP2A/MGMT signaling pathway plays important roles in temozolomide resistance in glioblastoma.

Temozolomide was recognized as the first-line therapy for glioblastoma to prolong the survival of patients noticeably, while recent clinical studies found that some patients were not sensitive to temozolomide treatment. The possible mechanisms seemed to be methylguanine-DNA-methyltransferase (MGMT), mismatch repair, PARP, etc. And the abnormal expression of MGMT might be the most direct factor.

Delivery of MGMT mRNA to glioma cells by reactive astrocyte-derived exosomes confers a temozolomide resistance phenotype.

The glioma-astrocyte interaction plays an important role in tumor microenvironment remodeling; however, the underlying mechanism has not been completely clarified. In this study, we show that glioma cells stimulate normal human astrocyte (NHA) into reactive astrocyte (RAS) in a non-contact manner. Additionally, the amount of O6-alkylguanine DNA alkyltransferase (MGMT) mRNA in exosomes (EXOs) released by RAS was significantly increased compared with that in non-reactive NHA.

EZH2 alteration driven by microRNA-524-5p and microRNA-324-5p promotes cell proliferation and temozolomide resistance in glioma.

Recent data have been shown that EZH2 is a critical oncogene via the repression of tumor suppressor genes in human cancers. In our study, we performed a genome-wide miRNA screen with a bioinformatics analysis to identify EZH2 specific miRNAs. Of these miRNAs, miR-524-5p and miR-324-5p were decreased in glioma tissues, and confered poor prognosis for glioma patients.

MicroRNA-520d-5p inhibits human glioma cell proliferation and induces cell cycle arrest by directly targeting PTTG1.

Glioma accounts for the majority of primary malignant brain tumors in adults and is highly aggressive. Although various therapeutic approaches have been applied, outcomes of glioma treatment remain poor. Acquiring a better understanding of the pathogenic mechanisms is essential to the design of effective therapeutic strategies.

Fstl1 Promotes Glioma Growth Through the BMP4/Smad1/5/8 Signaling Pathway.

Background: Gliomas result in the highest morbidity and mortality rates of intracranial primary central nervous system tumors because of their aggressive growth characteristics and high postoperative recurrence. They are characterized by genetic instability, intratumoral histopathological variability and unpredictable clinical behavior in patients. Proliferation is a key aspect of the clinical progression of malignant gliomas, complicating complete surgical resection and enabling tumor regrowth and further proliferation of the surviving tumor cells.

MicroRNA-141-3p promotes glioma cell growth and temozolomide resistance by directly targeting p53.

Glioblastoma multiforme is the most common primary malignancy in the brain and confers a uniformly poor prognosis. MicroRNAs have been shown to activate or inhibit tumorigenesis. Abnormalities in the p53 signaling pathway are found in various cancers and correlate with tumor formation.

Photoelectrocatalytic degradation of methylene blue using F doped TiO photoelectrode under visible light irradiation.

Photoelectrocatalysis (PEC) has attracted great interest due to cost effectiveness and high efficiency in water treatment. In this study, F doped TiO (F-TiO) photoelectrodes with honeycomb like morphology were prepared, and the PEC performance was investigated. F-TiO particles that showed enhanced absorption of visible light were synthesized via a sol-gel method.

MicroRNA-1301 inhibits proliferation of human glioma cells by directly targeting N-Ras.

Glioma is one of the most common, rapidly progressive and fatal brain tumors, and accumulating evidence shows that microRNAs (miRNAs) play important roles in the development of cancers, including glioma. Therapeutic applications of miRNAs in Ras-driven glioma have been proposed; however, their specific functions and mechanisms are poorly understood. Here, we report that miR-1301-3p directly targets the neuroblastoma Ras viral oncogene homolog (N-Ras) and functions as a tumor-suppressor in glioma.

MicroRNA-1468-5p inhibits glioma cell proliferation and induces cell cycle arrest by targeting RRM1.

MicroRNAs are associated with different types of cancers. In this study, we found that miR-1468-5p could inhibit growth and cell cycle progression in glioma by targeting ribonucleotide reductase large subunit M1 (RRM1). First, we analyzed miR-1468-5p expression in different glioma grades and the prognostic significance of its expression in glioblastoma multiform patients from the Chinese Glioma Genome Atlas.

CBX7 is a glioma prognostic marker and induces G1/S arrest via the silencing of CCNE1.

Chromobox homolog 7 (CBX7) cooperates with other polycomb group (PcG) proteins to maintain target genes in a silenced state. However, the precise role of CBX7 in tumor progression is still controversial. We found that the expression of CBX7 in four public databases was significantly lower in high grade glioma (HGG).

Polycomb group expression signatures in the malignant progression of gliomas.

Polycomb group (PcG) proteins form at least two key complexes, namely polycomb repressive complex 1 and polycomb repressive complex 2. These complexes are involved in the progression of various cancers. Systematic research has not been conducted on the aberrant expression of PcG members in gliomas.

MiR-198 enhances temozolomide sensitivity in glioblastoma by targeting MGMT.

Glioblastoma is one of the most frequent and aggressive brain tumors. Accumulating evidence indicates that microRNAs are involved in glioma proliferation, invasion and drug resistance. Previous studies showed that miR-198 is downregulated in glioblastoma.

Blocking MIR155HG/miR-155 axis inhibits mesenchymal transition in glioma.

Background: MIR155 host gene (MIR155HG) is a long noncoding RNA that has been considered as the primary micro (mi)RNA of miR-155. MIR155HG plays an essential role in hematopoiesis, inflammation, and tumorigenesis. Our study investigated the clinical significance, biological function, mechanisms, and small-molecule inhibitors of the MIR155HG/miR-155 axis in glioma.

Hypoxia induces H19 expression through direct and indirect Hif-1α activity, promoting oncogenic effects in glioblastoma.

H19 expression is elevated in many human tumors including glioblastomas, suggesting an oncogenic role for the long noncoding RNA; yet the upregulation of H19 in glioblastomas remains unclear. Here we report that hypoxia significantly stimulated H19 expression in glioblastoma cell lines, which was related to hypoxia-inducible factors 1α (Hif-1α). Hif-1α promoted H19 expression in U87 and U251 cells.

The malignancy of miR-18a in human glioblastoma via directly targeting CBX7.

Aberrant levels of microRNAs (miRNAs) are linked to tumorigenesis and tumor progression. Here we analyzed the expression of microRNA 18a in glioblastoma multiforme (GBM) within groups of coexpressed groups of genes through analysis of expression profiling databases and clinical tissues. Cell proliferation and flow cytometry experiments were performed to determine the roles of miR-18a in the proliferation of glioblastoma cells in vitro.

BACH1 Promotes Temozolomide Resistance in Glioblastoma through Antagonizing the Function of p53.

The acquisition of drug resistance is a persistent clinical problem limiting the successful treatment of glioblastoma (GBM). However, the molecular mechanisms by which initially chemoresponsive tumors develop therapeutic resistance remain poorly understood. In this study, we report that BACH1, a heme-binding protein that participates in transcriptional repression or activation, was significantly upregulated in glioblastoma tissues.