The function of glutamate ionotropic receptor NMDA type subunit 1 (GRIN1) in neurodegenerative diseases has been widely reported; however, its role in the occurrence of glioma remains less explored. We obtained clinical data and transcriptome data from the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA). Hub gene’s expression differential analysis and survival analysis were conducted by browsing the Gene Expression Profiling Interactive Analysis (GEPIA) database, Human Protein Atlas database, and LOGpc database. We conducted a variation analysis of datasets obtained from GEO and TCGA and performed a weighted gene coexpression network analysis (WGCNA) using the R programming language (3.6.3). Kaplan-Meier (KM) analysis was used to calculate the prognostic value of GRIN1. Finally, we conducted Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. Using STRING, we constructed a protein–protein interaction (PPI) network. Cytoscape software, a prerequisite of visualizing core genes, was installed, and CytoHubba detected the 10 most tumor-related core genes. We identified 185 differentially expressed genes (DEGs). GO and KEGG enrichment analyses illustrated that the identified DEGs are imperative in different biological functions and ascertained the potential pathways in which the DEGs may be enriched. The overall survival calculated by KM analysis showed that patients with lower expression of GRIN1 had worse prognoses than patients with higher expression of GRIN1 ( p = 0.004 ). The GEPIA and LOGpc databases were used to verify the expression difference of GRIN1 among GBM, LGG, and normal brain tissues. Ultimately, immunohistochemical assay results showed that GRIN1 was detected in normal tissue and not in the tumor specimens. Our results highlight a potential target for glioma treatment and will further our understanding of the molecular mechanisms underlying the treatment of glioma.
The present study aimed to investigate the underlying regulatory mechanism of MYCL proto-oncogene (MYCL) in triple-negative breast cancer (TNBC) progression. In vitro experiments were performed to confirm the functional roles of MYCL in TNBC, and its effects on the JAK/STAT3 pathway through flow cytometric analysis, colony formation, wound healing and Transwell assays. In addition, the GSE45498 dataset demonstrated that MYCL was upregulated in TNBC and that it was significantly related to poor survival of patients with TNBC. Knockdown of MYCL induced the apoptosis, and suppressed the proliferation, migration and invasion of TNBC cells by inhibiting the JAK/STAT3 pathway. Notably, MYCL could activate the JAK/STAT3 pathway, whereas inhibition of the JAK/STAT3 pathway could eliminate the effect of MYCL on TNBC cells. Knockdown of MYCL also suppressed the growth of TNBC xenograft tumors. In conclusion, MYCL could promote TNBC progression by activating the JAK/STAT3 pathway.
Cuproptosis is a newly discovered way of cell death which contributed to the accumulation of copper as well as targeting lipoylated TCA cycle proteins and what role that cuproptosis plays in ALS is still unknown. We analyzed 10 cuproptosis-related genes between ALS patients (233 samples) and non-ALS patients (508 samples) based on Gene Expression Omnibus (GEO) GSE112676. We constructed RF model to predict occurrence of ALS. By establishing coppercluster and gene cluster, we explored cuproptosis functioning patterns and immune cells infiltration in ALS and quantified these functioning patterns by erecting copperscore criterion. LIPT1, DLAT, DLD and PDHB were identified as differential expressed genes in ALS which high expression of them relates to pathogenicity of ALS. Moreover, T cell family, B cell family and dendritic family may highly be involved in the happening of ALS while mononuclear phagocyte system and nature killer cell family were silenced. Our findings provide potential immunotherapy and biomarkers to foresee the happening of ALS.
Breast cancer (BC), which is most commonly seen in women, has become the second most common cause of cancer death in the United States. The number of women dying from BC is increasing every year, especially in the developing countries that fall behind in terms of economy and technologies. Therefore, it is of great necessity to find potential targets to effectively treat this disease. In this study, RT-qPCR was performed to detect the expressions of TCL6, miR-665, and CD82. CCK-8 and immunofluorescence assays were conducted for the assessment of BC cell proliferation. The invasion and migration of BC cells were detected by transwell and wound healing assays, respectively. Luciferase reporter assay was used to verify the combination of TCL6 and miR-665, and the binding of miR-665 and CD82. Moreover, the proliferation and migration of related proteins were measured by western blot. The results showed that TCL6 was low expressed in BC cells, but overexpression of TCL6 inhibited the proliferation, migration, and invasion of BC cells. On the contrary, miR-665 was highly expressed in BC cells, while its expression was negatively correlated with TCL6 as suggested by RT-qPCR assay. Furthermore, the inhibitory effects of TCL6 overexpression on the proliferation, migration, and invasion of BC cells were reversed by miR-665 mimic. Afterwards, the binding sites between miR-665 and CD82 were verified by luciferase reporter assay. Overexpression of TCL6 increased the level of CD82 in BC cells, but this effect was reversed by miR-665 mimic as well. In conclusion, the present study has presented the fact that TCL6 could enhance the expression of CD82 by down-regulating the expression of miR-665.
Background Most studies related to N6-methyladenosine (m6A) in glioma have been conducted only at the single-gene level, while the m6A modification patterns and correlation between m6A and immune cells’ tumor microenvironment infiltration have not been comprehensively reported. Methods Eighty-five clinical samples were obtained from the Gene Expression Omnibus; another 599 clinical samples and 174 transcriptome data were obtained from The Cancer Genome Atlas. Based on data analysis using the R program and principal component analysis, we established an m6Ascore quantitative scoring system and analyzed the modification of 22 m6A-related genes with TME infiltration characteristics. Results Three m6A modification patterns and the characteristics of immune cell infiltration were identified. Cluster A corresponded to the immune-desert phenotype, cluster B corresponded to the immune-excluded phenotype, and cluster C corresponded to the immune-inflamed phenotype. Cluster B showed the worst long-term prognosis, whereas cluster A had the best long-term prognosis. Anti-CD52/HE5 shows potential as an immune therapy for glioma. Conclusions This research provides a foundation for understanding m6A modification patterns in glioma and a potential prognostic biomarker and immune therapy target for treat glioma.
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