N--acetyltransferase 10 protein (Naa10p, also called ARD1), the catalytic subunit of N-acetyltransferase A, is a critical regulator of cell death and proliferation. Naa10p is also shown to regulate cancer metastasis by inhibiting cell motility, however its role in cancer metastasis is not fully understood. In this study, we found that high expression of Naa10p is positively correlated with the survival of patients with breast cancer, while negatively correlated with lymph node metastasisr. Naa10p inhibits breast cancer cell migration and invasion in vitro and decreases the xenograft growth and metastasis in nude mice. Microarray screening revealed that Naa10p down-regulates expression of several pro-invasive genes, which was validated by qRT-PCR analysis.
Inhibition of STAT5a by Naa10p contributes to decreased breast cancer metastasis.
Cell line, Treatment
View SamplesTo exploit targets or signaling pathways affected by PLS-123 during anti-tumor process, gene expression profiling was carried out in representative OCI-Ly7 cells treated for 24 hours.
Irreversible dual inhibitory mode: the novel Btk inhibitor PLS-123 demonstrates promising anti-tumor activity in human B-cell lymphoma.
Specimen part, Cell line
View SamplesTo exploit targets or signaling pathways affected by PLS-123 during anti-tumor process, gene expression profiling was carried out in OCI-Ly7 inoculated xenograft model.
Irreversible dual inhibitory mode: the novel Btk inhibitor PLS-123 demonstrates promising anti-tumor activity in human B-cell lymphoma.
Specimen part
View SamplesChronic infection of M. hyorhinis is postulated to be associated with cancer cell migration and invasion. To explore the mechanisms of M. hyorhinis-promoted invasiveness, we performed Affymetrix genechip (HuGene-1_0-st) analysis to examine differential gene expression profiles between non-infected and infected gastric cancer cells.
No associated publication
Disease, Disease stage, Cell line
View SamplesFind the possible signaling pathways which contribute to the cell growth inhibition effect of SW-treated AGS cells
Sarsaparilla (Smilax Glabra Rhizome) Extract Inhibits Cancer Cell Growth by S Phase Arrest, Apoptosis, and Autophagy via Redox-Dependent ERK1/2 Pathway.
Sex, Specimen part, Disease
View SamplesTo find the possible signaling pathways which contribute to the anticancer effect of SW-treated HepG2 cells
No associated publication
Specimen part, Cell line
View SamplesIn proliferating cells, where most Polycomb repressive complex 2 (PRC2) studies have been performed, gene repression is associated with PRC2 trimethylation of H3K27 (H3K27me3). However, it is uncertain whether PCR2 writing of H3K27me3 is mechanistically required for gene silencing. Here we studied PRC2 function in postnatal mouse cardiomyocytes, where the paucity of cell division obviates bulk H3K27me3 rewriting after each cell cycle. EED (Embryonic Ectoderm Development) inactivation in the postnatal heart (Eed CKO ) caused lethal dilated cardiomyopathy. Surprisingly, gene upregulation in Eed CKO was not coupled with loss of H3K27me3. Rather, the activating histone mark H3K27ac increased. EED interacted with histone deacetylases (HDACs) and enhanced their catalytic activity. HDAC overexpression normalized Eed CKO heart function and expression of derepressed genes. Our results uncovered a non-canonical, H3K27me3-independent EED repressive mechanism that is essential for normal heart function. Our results further illustrate that organ dysfunction due to epigenetic dysregulation can be corrected by epigenetic rewiring.
EED orchestration of heart maturation through interaction with HDACs is H3K27me3-independent.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
A systematic analysis of the skeletal muscle miRNA transcriptome of chicken varieties with divergent skeletal muscle growth identifies novel miRNAs and differentially expressed miRNAs.
Specimen part
View SamplesThe genetic closeness and divergent muscle growth rates of broilers and layers make them great models for myogenesis study. In order to discover the molecular mechanisms determining the divergent muscle growth rates and muscle fiber sizes in different chicken lines, we systematically identified differentially expressed genes between broilers and layers during muscle development (embyonic day 10, 12, 14 and 18) by microarray hybridization experiment.
A systematic analysis of the skeletal muscle miRNA transcriptome of chicken varieties with divergent skeletal muscle growth identifies novel miRNAs and differentially expressed miRNAs.
Specimen part
View SamplesThe molecular explanation for tamoxifen serving as a breast cancer treatment but displaying partial estrogenic in the uterus is not known. Previously, we reported that differential promoter context and cofactor recruitment contribute to the tissue specificity of tamoxifen. Here, we investigated the genomic basis for the partial oestrogenic activity of tamoxifen in the endometrium. We showed that tamoxifen not only affects the rate of transcription of oestrogen target genes but also targets a unique set of genes. Since oestrogen and tamoxifen are both able to bind to oestrogen receptors (ERs) and because both promote endometrial carcinogenesis, we hypothesized that the molecular effectors for ERs in endometrial carcinogenesis most likely reside in genes that are commonly targeted by oestrogen and tamoxifen. Among those target genes, we identified a paired-box gene PAX2 that is critically involved in cell proliferation and carcinogenesis in the endometrium. Our experiments also demonstrated that PAX2 is activated by oestrogen and tamoxifen in endometrial carcinomas but not in normal endometrium, and this activation is associated with cancer-linked hypomethylation of the PAX2 promoter.
Hypomethylation-linked activation of PAX2 mediates tamoxifen-stimulated endometrial carcinogenesis.
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