GPR27 expression correlates with prognosis and tumor progression in gliomas.

Backgrounds: Glioma is a highly aggressive type of brain tumor, and its prognosis is still poor despite recent progress in treatment strategies. G protein-coupled receptor 27 (GPR27) is a member of the G protein-coupled receptor family and has been reported to be involved in various cellular processes, including tumor progression. Nevertheless, the clinical potential and tumor-related role of GPR27 in glioma remain unknown. Here we aimed to explore the function and role of GPR27 in gliomas. Methods: In the current study, we evaluated the expression and clinical significance of GPR27 in gliomas using data from The Cancer Genome Atlas (TCGA) datasets. We also conducted cellular experiments to evaluate the functional role of GPR27 in glioma cell growth. Results: We found that GPR27 expression level was closely associated with disease status of glioma. Of note, GPR27 was negatively correlated with WHO grade, with grade IV samples showing the lowest GPR27 levels, while grade II samples showed the highest levels. Patients with IDH mutation or 1p/19q co-deletion exhibited higher GPR27 levels. In addition, lower GPR27 levels were correlated with higher death possibilities. In cellular experiments, we confirmed that GPR27 inhibited glioma cell growth. Conclusions: Our results indicate that GPR27 may function as a potential prognostic biomarker and therapeutic target in gliomas. Further studies are needed to illustrate the signaling mechanism and clinical implications of GPR27 in gliomas.

Transmembrane and Ubiquitin-Like Domain-Containing 1 Promotes Glioma Growth and Indicates Unfavorable Prognosis.

Background: Ubiquitin-related proteins have garnered increasing attention for their roles in tumorigenesis. Transmembrane and ubiquitin-like domain-containing 1 (TMUB1) is a recently discovered protein in the ubiquitin-like domain family, yet its involvement in glioma remains poorly understood. This study is aimed at investigating the functional significance and clinical relevance of TMUB1 in glioma. Methods: We conducted a comprehensive analysis using two cohorts: a retrospective glioma cohort from our hospital and The Cancer Genome Atlas (TCGA) cohort. The mRNA levels of TMUB1 were assessed through reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Clinical associations of TMUB1 in these cohorts were evaluated using correlation tests, chi-square tests, and survival analyses. Additionally, we performed TMUB1 knockdown in U87 and LN-229 human glioma cell lines, and cellular growth was assessed through the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay. Results: Our results revealed that TMUB1 expression was elevated in glioma tissues compared to normal brain tissues. Notably, lower TMUB1 expression correlated with favorable characteristics such as lower World Health Organization (WHO) grade and 1p/19q codeletion. Moreover, patients with higher TMUB1 levels in glioma tissues exhibited worse prognosis in both TCGA cohort and our retrospective cohort, underscoring its prognostic significance in gliomas. Cellular experiments demonstrated that TMUB1 silencing suppressed the growth of glioma cells. Conclusions: TMUB1 emerges as a novel and clinically relevant prognostic biomarker for gliomas. Targeting TMUB1 holds promise as a potential strategy for glioma treatment. This study contributes valuable insights into the multifaceted role of TMUB1 in glioma pathogenesis and its potential as a diagnostic and therapeutic target.

Correlation between LSM1 Expression and Clinical Outcomes in Glioblastoma and Functional Mechanisms.

Background: Glioblastoma (GBM) is an aggressive form of brain tumor characterized by limited treatment options and a bleak prognosis. Although the role of Like-Sm 1 (LSM1), a component of the mRNA splicing machinery, has been studied in various cancers, its significance in GBM remains unclear. The purpose of this research was to investigate the expression of LSM1 and its role in driving GBM progression. Methods: We analyzed gene expression data obtained from TCGA and GTEx databases to compare the levels of LSM1 expression between GBM and normal brain tissues. To assess the impact of LSM1, we conducted experiments using U87 GBM cells, wherein we manipulated LSM1 expression through overexpression and knockdown techniques. These experiments allowed us to evaluate cellular behaviors such as proliferation and invasion. Additionally, we explored the correlation between LSM1 expression and immune cell infiltration in GBM. Results: Our analysis of TCGA and GTEx datasets revealed a significant upregulation of LSM1 expression in GBM compared to normal brain tissues. In our in vitro experiments using U87 cells, we observed that LSM1 overexpression promoted cell proliferation and invasion, while LSM1 knockdown exerted the opposite effects. Moreover, we discovered correlations between LSM1 expression and immune cell infiltration in GBM, specifically involving TFH cells, CD56bright cells, macrophages, and Th2 cells. Conclusions: The findings of this study demonstrate the upregulation of LSM1 in GBM and its contribution to tumor progression by enhancing cell proliferation, invasion, and influencing immune cell infiltration. Our research sheds light on the potential oncogenic role of LSM1 in GBM and suggests its viability as a therapeutic target for this aggressive brain tumor.

Role of P38 mitogen-activated protein kinase on Cx43 phosphorylation in cerebral vasospasm after subarachnoid hemorrhage.

OBJECTIVES: Cx43 phosphorylation is involved in the pathogenesis of cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH). However, the exact phosphorylation mechanism of Cx43 in CVS is not fully elucidated. Thus, we examined the role of P38MAPK in CVS and Cx43 phosphorylation, using a double hemorrhage rat model. METHODS: Sprague-Dawley rats weighing 300-350 g were grouped into sham, SAH, vehicle, and SAH + SB203580. SAH was induced by double injecting blood into the prechiasmatic cisterns. Neurological score was measured with the Garcia scoring system, and the diameters of basilar arteries and the expression of pCx43, pP38MAPK, and P38MAPK proteins were measured through pressure myograph measurement and Western blot analysis, respectively. RESULTS: The neurological scores remarkably decreased after SAH but remarkably improved after SB203580 was used. The results of pressure myograph analysis on the SAH and vehicle groups showed the considerable narrowing of the basilar arteries in comparison with that of the sham group. By contrast, the arterial diameters in the SAH + SB203580 group were much larger than those observed in the SAH and vehicle groups. Moreover, the P38MAPK expression in the sham group had no substantial change in contrast to the SAH and vehicle groups, and pCx43 and pP38MAPK increased in the SAH and vehicle groups. Meanwhile, the SAH + SB203580 group showed marked decrease in Cx43 and P38MAPK phosphorylation levels relative to the SAH and vehicle groups. CONCLUSIONS: P38MAPK pathway facilitates the development of CVS through the upregulation of Cx43 phosphorylation.