The clinical significance of glutathione peroxidase 2 in glioblastoma multiforme

Abstract Background Glioblastoma multiforme (GBM) is the leading cause of death among adult brain cancer patients. Glutathione peroxidase 2 (GPX2), as a factor in oxidative stress, plays an important role in carcinogenesis. However, its role in GBM has not been well established. The study aimed to investigate the clinical significance of GPX2 with GBM prognosis. Methods Data of GBM and healthy individuals were retrospectively collected from oncomine, cancer cell line encyclopedia (CCLE), gene expression profiling interactive analysis (GEPIA), UALCAN, and Human Protein Atlas. GPX2 mRNA expression was first assessed across various cancer types in oncomine and cancer cell lines from CCLE. The mRNA expression of GPX2 was compared between normal and GBM tissues using GEPIA (normal = 207; GBM = 163) and UALCAN (normal = 5; GBM = 156). The GPX2 methylation was analyzed using data from UALCAN (normal = 2; GBM = 140). The prognostic value of GPX2 in GBM was explored in GEPIA and UALCAN using Kaplan–Meier method. STRING database was used to construct protein–protein interaction (PPI) network and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway. Statistical significance was set as <0.05. Results The current study revealed no significant differences in GPX2 expression between normal and GBM from GEPIA data (P > 0.05) and UALCAN (P = 0.257). Patients with higher GPX2 intended to have a poorer prognosis (P = 0.0089). The KEGG pathways found that chemokine-signaling pathway were the more preferred. Conclusions The findings demonstrated that GPX2 might be a potential diagnosis and prognostic indicator for GBM. Chemokine-signaling pathway may be involved in GPX2 function.

Download Full-text

Role of JAK-STAT Pathway in Broiler Chicks Fed with Chestnut Tannins

Animals ◽

10.3390/ani11020337 ◽

2021 ◽

Vol 11 (2) ◽

pp. 337

Author(s):

Annah Lee ◽

Gabriela Cardoso Dal Pont ◽

Michele Battaglia ◽

Ryan J. Arsenault ◽

Michael H. Kogut

Keyword(s):

Mrna Expression ◽

Signaling Pathway ◽

Immune Modulation ◽

Cell Receptor ◽

Host Immunity ◽

Broiler Chicks ◽

Chemokine Signaling ◽

Chemokine Signaling Pathway ◽

Stat Pathway

The objective of this study was to identify the phosphorylation events associated with host immunity with the inclusion of chestnut tannins (ChT) in the diet. A total of 200 male day-of-hatch Cobb 500 chicks were randomly assigned to two treatment groups, totaling 50 chicks per pen per experiment (this study was repeated two times). The treatments were as follows: (1) control feed—normal starter feed (n = 50), and (2) 1% ChT inclusion feed (n = 50). The ceca were collected on each necropsy day for analysis via (1) a peptide array to provide tissue immunometabolism information from the host, and (2) quantitative PCR for mRNA expression. Of the top three immune pathways, the data identified the T-cell receptor signaling pathway, the chemokine signaling pathway, and the JAK-STAT signaling pathway. The results showed significantly altered phosphorylation of JAK and STAT peptides within the JAK-STAT pathway. These results support the mRNA expression data with the upregulated IL-6 response, due to the significant phosphorylation of IL6ST, JAK, and STAT peptides. In regard to immune modulation, ChT appear to influence host immunity via an IL-6 mediated response which could be beneficial in host defenses against pathogens at the early stages of broiler growth and development. Therefore, it is suggested that the role of the JAK-STAT pathway is altered by including ChT in the diet.

Download Full-text

Faculty Opinions recommendation of A Cxcl12-CXCR4 chemokine signaling pathway defines the initial trajectory of mammalian motor axons.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1027804.335791 ◽

2005 ◽

Author(s):

Harukazu Nakamura

Keyword(s):

Signaling Pathway ◽

Motor Axons ◽

Chemokine Signaling ◽

Chemokine Signaling Pathway

Download Full-text

Biomolecular network-based synergistic drug combination discovery: a combination of paeoniflorin and liquiritin alleviates neuropathic pain by inhibiting neuroinflammation via suppressing the chemokine signaling pathway

Signal Transduction and Targeted Therapy ◽

10.1038/s41392-020-0160-8 ◽

2020 ◽

Vol 5 (1) ◽

Cited By ~ 1

Author(s):

Qiuyan Guo ◽

Weijie Li ◽

Chao Wang ◽

Xia Mao ◽

Xiaoyue Wang ◽

...

Keyword(s):

Neuropathic Pain ◽

Signaling Pathway ◽

Drug Combination ◽

Chemokine Signaling ◽

Biomolecular Network ◽

Chemokine Signaling Pathway

Download Full-text

Investigation of Potential Genetic Biomarkers and Molecular Mechanism of Ulcerative Colitis Utilizing Bioinformatics Analysis

10.21203/rs.2.13329/v1 ◽

2019 ◽

Author(s):

Jiaqi Zhang ◽

Xue Wang ◽

Lin Xu ◽

Zedan Zhang ◽

Fengyun Wang ◽

...

Keyword(s):

Ulcerative Colitis ◽

Gene Therapy ◽

Inflammatory Response ◽

Signaling Pathway ◽

Functional Enrichment ◽

Hub Genes ◽

Amyloid A ◽

Chemokine Signaling ◽

Chemokine Signaling Pathway ◽

Potential Biomarkers

Abstract Objectives: To reveal the molecular mechanisms of ulcerative colitis (UC) and provide potential biomarkers for UC gene therapy. Methods: We downloaded the GSE87473 microarray dataset from the Gene Expression Omnibus (GEO) and identified the differentially expressed genes (DEGs) between UC samples and normal samples. Then ,a module partition analysis was performed based on a weighted gene co-expression network analysis (WGCNA),followed by pathway and functional enrichment analyses. Furthermore, we investigated the hub genes . At last, data validation was performed to ensure the reliability of the hub genes. Results: Between UC group and normal group, 988 DEGs were investigated . The DEGs were clustered into 5 modules using WGCNA. These DEGs were mainly enriched in functions such as the immune response, the inflammatory response and chemotaxis, and they were mainly enriched in KEGG pathways such as the cytokine-cytokine receptor interaction , chemokine signaling pathway, and complement and coagulation cascades. The hub genes, including dual oxidase maturation factor 2(DUOXA2), serum amyloid A (SAA) 1 and SAA2, TNFAIP3-interacting protein 3(TNIP3), C-X-C motif chemokine (CXCL1), solute carrier family 6 member 14(SLC6A14) and complement decay-accelerating factor (CD antigen CD55),were revealed as potential tissue biomarkers for UC diagnosis or treatment. Conclusions: This study provides supportive evidence that DUOXA2, A-SAA, TNIP3, CXCL1, SLC6A14 and CD55 might be used as potential biomarkers for tissue biopsy of UC, especially SLC6A14 and CD55, which may be new targets for UC gene therapy. Moreover, the DUOX2/DUOXA2, NF-κB /TNIP3 and CXCL1/CXCR2 pathways might play an important role in the progression of UC through the chemokine signaling pathway and inflammatory response.

Download Full-text

Upregulated C-C Motif Chemokine Ligand 2 Promotes Ischemic Stroke via Chemokine Signaling Pathway

Annals of Vascular Surgery ◽

10.1016/j.avsg.2020.04.047 ◽

2020 ◽

Vol 68 ◽

pp. 476-486

Author(s):

Lin Li ◽

Weimin Lou ◽

Hailong Li ◽

Yuehong Zhu ◽

Xiong’ang Huang

Keyword(s):

Ischemic Stroke ◽

Signaling Pathway ◽

Chemokine Signaling ◽

Chemokine Ligand ◽

Chemokine Signaling Pathway ◽

Chemokine Ligand 2

Download Full-text

Low-level laser irradiation treatment reduces CCL2 expression in rat rheumatoid synovia via a chemokine signaling pathway

Lasers in Medical Science ◽

10.1007/s10103-011-0917-y ◽

2011 ◽

Vol 26 (5) ◽

pp. 707-717 ◽

Cited By ~ 20

Author(s):

Lin Zhang ◽

Jian Zhao ◽

Noboru Kuboyama ◽

Yoshimitsu Abiko

Keyword(s):

Laser Irradiation ◽

Signaling Pathway ◽

Low Level ◽

Low Level Laser ◽

Chemokine Signaling ◽

Level Laser ◽

Ccl2 Expression ◽

Irradiation Treatment ◽

Chemokine Signaling Pathway ◽

Low Level Laser Irradiation

Download Full-text

Specific Differentially Methylated and Expressed Genes in People with Longevity Family History

Iranian Journal of Public Health ◽

10.18502/ijph.v50i1.5082 ◽

2021 ◽

Author(s):

Chunhong LI ◽

Qingqing NONG ◽

Bin GUAN ◽

Haoyu HE ◽

Zhiyong ZHANG

Keyword(s):

Family History ◽

Signaling Pathway ◽

Killer Cell ◽

Cell Receptor ◽

Human Longevity ◽

Chemokine Signaling ◽

Differentially Methylated Genes ◽

Receptor Signaling Pathway ◽

Chemokine Signaling Pathway ◽

And Control

Background: We attempt to identify specific differentially methylated and expressed genes in people with longevity family history, it will contribute to discover significant features about human longevity. Methods: A prevalence study was conducted during October 2017 to January 2019 in Bama County of Guangxi, China and individuals were recruited and grouped into longevity family (n=60) and non-longevity family (n=60) to identify differentially methylated genes (DMGs). The expression profile dataset GSE16717 was downloaded from the GEO database in which individuals were divided into 3 groups, namely longevity (n=50), longevity offspring (n=50) and control (n=50) for identifying differentially expressed genes (DEGs). It was considered significantly different when P or adjusted P0.05. Results: In total, 117 longevity-related hypermethylated genes enriched in interleukin secretion/production regulation, chemokine signaling pathway and natural killer cell-mediated cytotoxicity. Another 296 significant key longevity-related DEGs primarily involved in protein binding, nucleus, cytoplasm, T cell receptor signaling pathway and Metabolic pathway, H19 and PFKFB4 were found to be both methylated and downregulated in people with longevity family history. Conclusion: Human longevity-specific genes involve in many immunity regulations and cellular immunity pathways, H19 and PFKFB4 show hypermethylated and suppressed status in people with longevity family history and might serve as longevity candidate genes.

Download Full-text

Mutational burden of hepatoblastomas: a role for the CX3CL1/CX3CR1 chemokine signaling pathway

10.1101/555466 ◽

2019 ◽

Author(s):

Talita Ferreira Marques Aguiar ◽

Maria Prates Rivas ◽

Silvia Costa ◽

Tatiane Rodrigues ◽

Juliana Sobral de Barros ◽

...

Keyword(s):

Signaling Pathway ◽

Tumor Cells ◽

Somatic Mutations ◽

Chemotherapy Response ◽

Mutational Signature ◽

Relative Paucity ◽

Chemokine Signaling ◽

Cancer Types ◽

Negative Tumor ◽

Chemokine Signaling Pathway

ABSTRACTBackgroundHepatoblastoma is an embryonal liver tumor supposed to arise from the impairment of hepatocyte differentiation during embryogenesis. CTNNB1 is the only recurrently mutated gene, and this relative paucity of somatic mutations poses a challenge to risk stratification and development of targeted therapies.MethodsIn this study, we investigated by exome sequencing the burden of somatic mutations in a cohort of 10 hepatoblastomas, including a congenital case.ResultsOur data disclosed a low mutational background with only three recurrently mutated genes: CTNNB1 and two novel candidates, CX3CL1 and CEP164. The major finding was a recurrent mutation (A235G) identified in two hepatoblastomas at the CX3CL1 gene; evaluation of RNA and protein expression revealed up-regulation of CX3CL1 in tumors. The analysis was replicated in two independents cohorts, substantiating that an activation of the CX3CL1/CX3CR1 pathway occurs in hepatoblastomas, with a predominance of these proteins in the cytoplasm of tumor cells. These proteins were not detected in the infiltrated lymphocytes of inflammatory regions of the tumors, in which they should be expressed in normal conditions, whereas necrotic regions exhibited negative tumor cells, but strongly positive infiltrated lymphocytes. Our data suggested that CX3CL1/CX3CR1 upregulation may be a common feature of hepatoblastomas, potentially related to chemotherapy response and progression. In addition, three mutational signatures were identified in hepatoblastomas, two of them with predominance of either the COSMIC signatures 1 and 6, found in all cancer types, or the COSMIC signature 29, related only with tobacco chewing habit; a third novel mutational signature presented an unspecific pattern with an increase of C>A mutations.ConclusionsOverall, we present here evidence that CX3CL1/CX3CR1 chemokine signaling pathway is likely involved with hepatoblastoma tumorigenesis or progression, besides reporting a novel mutational signature specific to a hepatoblastoma subset.

Download Full-text

Mutations Status of Chemokine Signaling Pathway Predict Prognosis of Immune Checkpoint Inhibitors in Colon Adenocarcinoma

Frontiers in Pharmacology ◽

10.3389/fphar.2021.721181 ◽

2021 ◽

Vol 12 ◽

Author(s):

Anqi Lin ◽

Wentao Xu ◽

Peng Luo ◽

Jian Zhang

Keyword(s):

Signaling Pathway ◽

Immune Checkpoint ◽

Immune Checkpoint Inhibitors ◽

Checkpoint Inhibitors ◽

Colon Adenocarcinoma ◽

Cox Regression Analysis ◽

Chemokine Signaling ◽

Number Of Patients ◽

Chemokine Signaling Pathway ◽

The Relationship

In recent years, tumor immunotherapy has become an important treatment program and popular research focus. However, the use of immune checkpoint inhibitors (ICI) in the treatment of colorectal cancer still has limitations due to the current markers only being able to predict the prognosis of a small number of patients. As the chemokine signaling pathway can promote the anti-tumor response of the immune system by recruiting immune cells, we explored the relationship between mutations in the chemokine signaling pathway and the prognosis of colon adenocarcinoma (COAD) patients receiving ICI treatment. To analyze the relationship between chemokine mutation status and the prognosis of patients receiving ICI treatment, clinical and mutation data, with immunotherapy, for a COAD cohort was obtained from “cbioportal.” Then, combining this with COAD cohort data from The Cancer Genome Atlas (TCGA) database, the panorama of gene mutation, immunogenicity, and difference in tumor microenvironment (TME) of chemokine pathways with different mutation statuses were analyzed. High-mut status has been proved to be a prognostic indicator of COAD patients receiving ICI treatment by Univariate and Multivariate Cox regression analysis. CIBERSORT analysis showed that the infiltration degree of M1 macrophages, neutrophils, and activated natural killer (NK) cells was higher in those with high-mut status. Immunogenicity of the high-mut group was also significantly increased, with the mutation number of tumor mutation burden (TMB), neoantigen load (NAL), DNA damage repair (DDR) pathway and microsatellite instability biomarker (MSI-H) being significantly higher. In this study, we found that the mutation state of chemokine pathways is closely associated with the prognosis of COAD patients undergoing ICI treatment. The higher number of TMB, NAL, and DDR mutations and inflammatory TME, may be the mechanism of behind a better prognosis. This discovery provides a possible idea for ICI therapy of COAD.

Download Full-text