Expression data from cell lines forced expressed PGC7/Stella
Ontology highlight
ABSTRACT: Global DNA hypomethylation and DNA hypermethylation of promoter regionsâincluding tumor suppressor genesâare frequently detected in human cancers. Although many studies have suggested a contribution to carcinogenesis, it is still unclear whether the aberrant DNA hypomethylation observed in tumors is a consequence or a cause of cancer. We found that overexpression of Stella (also known as PGC7, Dppa3), a maternal factor required for the maintenance of DNA methylation in early embryos, induced global DNA hypomethylation and transformation in NIH3T3 cells. This hypomethylation was due to the binding of Stella to Np95 (also known as Uhrf1, ICBP90) and the subsequent impairment of Dnmt1 localization. In addition, enforced expression of Stella enhanced the metastatic ability of B16 melanoma cells through the induction of metastasis-related genes by inducing DNA hypomethylation of their promoter regions. Such DNA hypomethylation itself causes cellular transformation and metastatic ability. These data provide new insight into the function of global DNA hypomethylation in carcinogenesis. We used microarrays to detail the global programme of gene expression by PGC7/Stella overexpression. RNA was extracted from NIH3T3 or B16F10 murine cell lines overexpressed PGC7/Stella and was hybridized on Affymetrix microarrays. We compared gene expression levels between control and PGC7/Stella-overexpressed cells. Microarray analysis was performed in NIH3T3 cells including two independent Stella-expressing NIH3T3 clones and a mixture of Stella-expressing NIH3T3 clones and in B16-F10 cells including three independent Stella-expressing B16-F10 clones.
Project description:Global DNA hypomethylation and DNA hypermethylation of promoter regions—including tumor suppressor genes—are frequently detected in human cancers. Although many studies have suggested a contribution to carcinogenesis, it is still unclear whether the aberrant DNA hypomethylation observed in tumors is a consequence or a cause of cancer. We found that overexpression of Stella (also known as PGC7, Dppa3), a maternal factor required for the maintenance of DNA methylation in early embryos, induced global DNA hypomethylation and transformation in NIH3T3 cells. This hypomethylation was due to the binding of Stella to Np95 (also known as Uhrf1, ICBP90) and the subsequent impairment of Dnmt1 localization. In addition, enforced expression of Stella enhanced the metastatic ability of B16 melanoma cells through the induction of metastasis-related genes by inducing DNA hypomethylation of their promoter regions. Such DNA hypomethylation itself causes cellular transformation and metastatic ability. These data provide new insight into the function of global DNA hypomethylation in carcinogenesis. We used microarrays to detail the global programme of gene expression by PGC7/Stella overexpression.
Project description:Genome-wide DNA methylation profiling of the human STELLA (hSTELLA) knockout cell clones derived from TGCT cell lines (BeWo and NCCIT). The DNA methylome profiles are also studied on the CRC cells lines (HCT116 and RKO) stably expressing hSTELLA and mouse STELLA (mSTELLA), as well as on the HCT116 cells treated by LNP-delivered mRNA encoding mSTELLA. The Infinium MethylationEPIC 850k array was used to obtain DNA methylation profiles across more than 850,000 CpGs in 26 samples. Samples included 6 cell clones derived from BeWo cells with hSTELLA knockout or sgRNA control, 5 cell clones derived from NCCIT cells with hSTELLA knockout or sgRNA control, 6 stable CRC cells expressing STELLA orthologs, and 9 LNP-mRNA treated HCT116 cells.
Project description:identify the potential partners of STC1 at the protein level, we performed mass spectrometry on B16-F10 tumor cells stably expressing FLAG-tagged STC1.
Project description:Three types of stimuli -- heat shock, Lipofectamine 2000 and benzyl alcohol -- induce activity of some stress genes (hsp) in mouse B16-F10 cells. Besides hsp genes induction, each stimulus causes gene expression changes of different sets of genes. We used microarrays to analyze global gene expression changes in mouse B16-F10 cells treated with elevated temperature (heat shock, HS), with Lipofectamine 2000 (LA) or with 40mM benzyl alcohol (BA).
Project description:Comparison of Macrophages from lungs 24hrs post-injection with B16-F10 Melanoma Cells expressing the Fluoresence Protein ZsGreen. ZsGreen+ and ZsGreen- macrophages were sorted and transcriptome compared.
Project description:Proteome analysis of Lung tissue of mice bearing B16-F10-luc-G5 melanoma tumor with sleep fragmentation and with or with out the asdmistration of GL-pp. The mice were randomly divided into 4 groups: control group in general condition with no further treatment (CON group), tumor group with the burden of B16-F10-luc-G5 cells (Tumor group), T+SF group with SF and the burden of B16-F10-luc-G5 cells (T+SF group), and GL-pp group with SF, tumor cells burden, and the administration of 80 mg/kg GL-pp (GL-pp group). B16-F10-luc-G5 cells (5 × 1000000 cells/100 µL per mouse) were injected into the mice through the tail vein. The lung tissue of T+SF group and GL-pp group were analyzed by the proteome.
Project description:Three types of stimuli -- heat shock, Lipofectamine 2000 and benzyl alcohol -- induce activity of some stress genes (hsp) in mouse B16-F10 cells. Besides hsp genes induction, each stimulus causes gene expression changes of different sets of genes. We used microarrays to analyze global gene expression changes in mouse B16-F10 cells treated with elevated temperature (heat shock, HS), with Lipofectamine 2000 (LA) or with 40mM benzyl alcohol (BA). In order to study how lipofection may affect cellular homeostasis, we used Affymetrix microarrays to analyze the whole transcriptome of mouse B16-F10 cells treated with Lipofectamine 2000. To find out which genes are affected, we compared the cells treated with Lipofectamine (LA1, LA2, LA3), the cells treated with 40mM benzyl alcohol (BA1, BA2, BA3), heat-shocked cells (HS1, HS2, HS3) and control, untreated cells (C1-5). RNA was extracted from cells 30 min after treatment.
Project description:We previously showed that transgenic enhancement of histamine production in B16-F10 melanomas strongly supports tumor growth in C57Bl/6 mice (Cancer Res, 2005 Pos et al.). In this array experiment, gene expression profiles of transgenic mouse melanomas, secreting different amounts of histamine, were compared by whole genome microarrays. Experiment Overall Design: By modifying the levels of L-histidine decarboxylase (HDC), the sole enzyme responsible for histamine production, we introduced three novel variants of the B16-F10 mouse melanoma cell line, displaying diminished (B16-F10 HDC-A), unmodified (B16-F10 HDC-M) or enhanced (B16-F10 HDC-S) capacities to produce and secrete histamine. Experiment Overall Design: In this experiment, B16-F10 HDC-A, HDC-M, and HDC-S experimental mouse melanomas were compared by analyzing 6-6 tumors in each group. Experiment Overall Design: In order to reduce the amount of arrays required, equal amounts of randomly chosen RNA sample pairs were pooled in each group, thus, at the end, each group consisted of 3 pooled tumor samples. All samples were biological replicates, no technical replicates or dye swapping were done. Experiment Overall Design: Gene expression patterns of the three tumor groups were compared indirectly, via a common reference samplei n a two-color array design. Arrays shown here represent gene expression patterns of individual tumor samples compared to the reference sample.
Project description:IRF4 deficient NK cells displayed more resistant to exhaustion during B16-F10 metastasis, to investigate how IRF4 deletion enhances the resistance of NK cells to exhaustion, we sorted NK cells from WT and Irf4-/- mice ingected with B16-F10 or not for RNA-seq