Ginsenoside Rg5 induces G2/M phase arrest, apoptosis and autophagy via regulating ROS-mediated MAPK pathways against human gastric cancer

Jumonji domain-containing protein 3 (JMJD3/KDM6B) demethylates lysine 27 on histone H3 (H3K27me3), a repressive epigenetic mark controlling chromatin organization and cellular senescence. To better understand the functional consequences of JMJD3 its expression was investigated in brain tumor cells. Querying patient expression profile databases confirmed JMJD3 over-expression in high-grade glioma. Immunochemical staining of two glioma cell lines, U251 and U87, indicated intrinsic differences in JMJD3 expression levels that were reflected in changes in cell phenotype and variations associated with cellular senescence, including senescence-associated beta-galactosidase (SA-beta-gal) activity and the senescence associated secretory phenotype (SASP). Over-expressing wild type JMJD3 (JMJD3wt) activated SASP-associated genes, enhanced SA-beta-gal activity, and induced nuclear blebbing. Conversely, over-expression of a catalytically inactive dominant negative mutant JMJD3 (JMJD3mut) increased proliferation. In addition, a large number of transcripts were identified by RNA-seq as altered in JMJD3 over-expressing cells, including cancer- and inflammation-related transcripts as defined by IPA analysis. These results suggest that expression of the SASP in the context of cancer undermines normal tissue homeostasis and contributes to tumorigenesis and tumor progression. These studies are therapeutically relevant because inflammatory cytokines have been linked to homing of neural stem cells and other stem cells to tumor loci. 

Implications: This glioma study brings together actions of a normal epigenetic mechanism (JMJD3 activity) with dysfunctional activation of senescence-related processes including secretion of SASP pro-inflammatory cytokines and stem cell tropism towards tumors.

https://mcr.aacrjournals.org/content/molcanres/early/2015/02/10/1541-7786.MCR-13-0268.full.pdf

The histone demethylase jumonji coordinates cellular senescence including secretion of neural stem cell-attracting cytokines.

Eosinophil associated genes in the inflammatory bowel disease 4 region: Correlation to inflammatory bowel disease revealed

Eosinophil associated genes in the inflammatory bowel disease 4 region: correlation to inflammatory bowel disease revealed.

OBJECTIVE It is unclear whether differentiation disturbances or deregulation of neural stem cells (NSCs) are the early key steps for gliomagenesis and tumor development. Furthermore, relevant molecular changes and gene-regulation pathways are unknown. This study focused on screening and validating differentiation-associated genes from both human NSCs and glioma cells with malignant progression, for the purpose of offering an experimental basis for the cellular origin of gilomas and molecular pathology of gliomagenesis. METHODS The differential-gene expression profiles of malignant progression of gliomas were established, then the differentiation related genes were screened out with a bioinformatics analysis. Expression levels of these genes was further analyzed in cultured human fetal NSCs undergoing differentiation processes with a semi-quantitative RT-PCR assay. RESULTS Eight genes were screened out from the gene-expression profiling of which the expression levels were associated with the differentiation processes of NSCs, namely CXCR4, TN-C, GLT1, IL1-RI, EGFR-8, CDC2, Ndr3 and MAPKK4. Three of them, ie., GLT1, CDC2 and MAPKK4, were further analyzed, showing that expression levels decreased with the differentiation processes of NSCs, and increased with the malignant progression of ganglioglioma. CONCLUSION Three differentiation associated genes were found negatively associated with NSCs differentiation and positively associated with malignant progression of gliomas, suggesting that differentiation disturbances of neural stem cells may be involved in oncogenesis, and that further studies on their roles in gliomagenesis should be conducted.

http://www.cancerbiomed.org/index.php/cocr/article/download/806/851

Molecular Study on Differentiation-Associated Genes Involved in Both Malignant Progression of Glioma and Differentiation of Human Fetal Neural Stem Cells

BACKGROUND & OBJECTIVE Exploiting the transcriptional regulation mechanism by microarray and bioinformatics is an important method at genomic research field, and it is better than previous methods, by which we can easily analyze the gene expression regulative networks at genomic level. This study was designed to analyze the glioma gene expression profiles by clustering and bioinformatic retrieving to seek some tumor development relative genes that can be cloned for the purpose of function research in the future. METHODS Firstly, we analyzed the glioma gene expression profiles of 16,363 genes by clustering, and chose 368 genes which expression differences were greater than 2 folds and the variances of 2 dots were smaller than 0.33. We selected 2 groups of genes that were expressed similarly. One group (11 cases) was upregulated with the glioma development and another (6 cases) was downregulated with the glioma development. Secondly, we determined the genomic information about those 17 genes and exploited their association with the development of gliomas. RESULTS Two groups of genes were expressed similarly during the glioma development, one group was upregulated with the development of gliomas, and another was downregulated. Bioinformatic analysis showed that 3 of those genes (X55987, M85085, and AB011097) might be important tumor relative genes. CONCLUSION By bioinformatics and microarray technologies, we found 3 genes, X55987(EDN, eosinophil-derived neurotoxin), AB011097 (ARTS-1, TNF receptor shedding regulator),and M85085(CStF, cleavage stimulation factor), which might be potential key tumor development relative genes that can be developed for therapy targets in the future.

Bioinformatic analysis of glioma development relative genes

Objective: To establish gene expression profiles associated with malignant progression of ganglioglioma. Methods: The primary and two recurrent glioma specimens were collected intraoperatively from the same patient who experienced tumor transformation into anaplastic astrocytoma and glioblastoma multiform for the first and second recurrence respectively. Gene expression was assayed through cDNA array and bioinformatics analysis. Results: A total of 197 differentially expressed genes with differential ratio value more than 3 compared with normal brain tissue were obtained. Among 109 functionally denned genes, those associated with development ranked the first by frequency, followed by genes associated with metabolism, differentiation, signal transduction and so on. As a result of cluster analysis among 368 genes, eleven genes were up regulated with malignant progression, while six genes were down regulated. Conclusion: Gene expression profiles associated with malignant progression of glioma were successfully established, which provides a powerful tool for research on molecular mechanisms of malignant progression of gliomas.

GENE EXPRESSION PROFILING OF GANGLIOGLIOMA MALIGNANT PROGRESSION BY cDNA ARRAY

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Bioinformatic analysis of glioma development relative genes

GENE EXPRESSION PROFILING OF GANGLIOGLIOMA MALIGNANT PROGRESSION BY cDNA ARRAY