AnxA4 expression is increased in H. pylori associated tumors. Moreover, in renal-cell cancer, AnxA4 increases tumor cell dissemination and promotes cell migration, and in colorectal cancer, it is identified as a potential diagnostic marker. How AnxA4 might be involved in tumorgenesis has remained unclear.
Revealing the molecular mechanism of gastric cancer marker annexin A4 in cancer cell proliferation using exon arrays.
Cell line, Treatment
View SamplesWe used microarrays to determine the expression profile of the P. aeruginosa creBC mutant regarding its parental wild type strain PAO1.
The Pseudomonas aeruginosa CreBC two-component system plays a major role in the response to β-lactams, fitness, biofilm growth, and global regulation.
Treatment
View SamplesWe reported that both conventional and adipose-specific Naa10p deletions in mice result in increased energy expenditure, thermogenesis, beige adipocyte differentiation and activation. Mechanistically, Naa10p acetylates the N-terminus of Pgc1α and prevents it from interacting with Ppar𝛾 to activate key genes, such as Ucp1, involved in beige adipocyte function. We used microarrays to profile the gene expression changes by Naa10p KO in inguinal white adipose tissues (iWATs) derived from mice fed with high fat diet for 15 weeks.
Naa10p Inhibits Beige Adipocyte-Mediated Thermogenesis through N-α-acetylation of Pgc1α.
Sex, Specimen part
View SamplesThe elevation of guanine nucleotide binding protein alpha 12 (G12) expression is highly associated with tumor invasiveness in several human cancers. We used an siRNA strategy to deplete G12 in oral squamous cell carcinoma (OSCC) cells and analyze the transcriptome profile by the Affymetrix Human Exon 1.0 ST platform.
Gα₁₂ drives invasion of oral squamous cell carcinoma through up-regulation of proinflammatory cytokines.
Sex, Specimen part, Cell line
View SamplesThis study focus on the expression signature between tumor and adjacent normal tissues.
Protein arginine methyltransferase 5 is a potential oncoprotein that upregulates G1 cyclins/cyclin-dependent kinases and the phosphoinositide 3-kinase/AKT signaling cascade.
Age
View SamplesA lung cancer cell model of invasive transformation was developed to select progressively invasive cell populations from a parental cell line of human lung adenocarcinoma, CL1. Five progressive sub-clones namely, CL1-1, CL1-2, CL1-3 CL1-4, and CL1-5 were selected using transwell and displayed increasing invasion potential (Chu et al, 1997).
Fucosyltransferase 8 as a functional regulator of nonsmall cell lung cancer.
Specimen part
View SamplesIn order to identify patterns of gene expression associated with biological effects in THP-1 cells induced by F3, we performed a transcriptomic analysis on the THP-1 control and F3-treated THP-1 cells by oligonucleotide microarray
Ganoderma lucidum polysaccharides in human monocytic leukemia cells: from gene expression to network construction.
Cell line
View SamplesProgressive failure of insulin-producing beta cells is the central event leading to diabetes, yet the signalling networks controlling beta cell fate remain poorly understood. Here we show that SRp55, a splicing factor regulated by the diabetes susceptibility gene GLIS3, has a major role in maintaining function and survival of human beta cells. RNA-seq analysis revealed that SRp55 regulates the splicing of genes involved in cell survival and death, insulin secretion and JNK signalling. Specifically, SRp55-mediated splicing changes modulate the function of the pro-apoptotic proteins BIM and BAX, JNK signalling and endoplasmic reticulum stress, explaining why SRp55 depletion triggers beta cell apoptosis. Furthermore, SRp55 depletion inhibits beta cell mitochondrial function, explaining the observed decrease in insulin release. These data unveil a novel layer of regulation of human beta cell function and survival, namely alternative splicing modulated by key splicing regulators such as SRp55 that may crosstalk with candidate genes for diabetes. Overall design: Five independent preparations of EndoC-ßH1 cells exposed to control (siCTL) or SRp55 (siSR#2) siRNAs
SRp55 Regulates a Splicing Network That Controls Human Pancreatic β-Cell Function and Survival.
Treatment, Subject
View SamplesEngraftment of primary pancreas ductal adenocarcinomas (PDAC) in mice to generate patient derived xenograft (PDX) models is a promising platform to for biological and therapeutic studies in this disease. However, these models are still incompletely characterized. Here, we measured the impact of the murine environment on the gene expression of the engrafted human tumoral cells. We have analyzed gene expression profiles from 35 new PDX models and compared them with previously published microarray data from PDAC and hepatocellular carcinoma (HCC). Our results showed that PDX models derived from PDAC, or HCC, were clearly different to the cell lines derived from the same cancer tissues. Indeed, PDAC- and HCC-derived cell lines are indistinguishable one from the other based in their gene expression profiles. In contrast, the transcriptomes of PDAC and HCC PDX models are clearly different and more similar to their original tumor than to PDX models from the other tumor type. Interestingly, the main differences between pancreatic PDX models and human PDAC is the expression of genes involved in pathways related with extracellular matrix interactions and cell cycle regulation likely reflecting the adaptations of the tumors to the new environment. Furthermore, most of these differences are detected in the first passages after the tumor engraftment, indicating early phases of the adaptation process. In conclusion, different from conventional cancer cell lines, PDX models of PDAC retain similar gene expression profiles of PDAC. Expression changes are mainly related to genes involved in stromal pathways likely reflecting the adaptation to new environments. We also provide evidence of the stability of gene expression patterns over subsequent passages.
Transcriptional dissection of pancreatic tumors engrafted in mice.
Specimen part
View SamplesSelective genetic ablation of the SIRT1 deacetylase domain in skeletal muscle results in increased H4K16 acetylation and deregulated activation of the myogenic program in satellite cells Overall design: To establish the role of the deacetylase SIRT1 in skeletal muscle we examined the genome wide distribution of H4K16ac in quiescent (FI) and proliferating (Cul) satellite cells isolated from WT mice (C57Bl/6 background) and SIRT1mKO (generated via breeding of Pax7cre/+ knock-in mice with mice containing the floxed exon 4 SIRT1 allele). We also analyzed the distribution of SIRT1 in quiescent and proliferating FACS isolated WT satellite cells (two replicates). We generated the mRNA profiles (at least two replicate for each experiment) of FACS isolated quiescent, proliferating and differentiating (1 day in differentiation medium) satellite cells of WT mice and SIRT1mKO. The selective genetic ablation of the SIRT1 deacetylase domain in skeletal muscle results in increased H4K16 acetylation and deregulated activation of the myogenic program.
The NAD(+)-dependent SIRT1 deacetylase translates a metabolic switch into regulatory epigenetics in skeletal muscle stem cells.
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