ARR (Adamantyl Retinoid Related molecules)-miRNA-Cancer
Ontology highlight
ABSTRACT: The adamantly-substituted retinoid related (ARR) molecules have been found to induce apoptosis in a variety of malignant cells both in vitro and in vivo. A number of mechanisms have been proposed by which apoptosis is achieved by this class of molecules. We have previously demonstrated that ARRs are potent inducers of apoptosis in leukemia and pancreatic cancer cells. We designed experiments that the exposure of leukemia and pancreatic cancer cell lines to the 3-Cl-AHPC ((E)-4-[3-(1-adamantyl)-4-hydroxyphenyl]-3-chlorocinnamic acid )may result in the modulation of microRNA expression or repression and that this differential microRNA expression may contribute to ARR-mediated inhibition of cellular proliferation and cell death induction.
Project description:Compare gene expression between maize genotype resistant (Pa405) and susceptible (Oh28) to maize dwarf mosaic virus (MDMV) infection 4 days post-inoculation using microarrays.
Project description:90K Combimatrix gene expression microarrays were composed by 17,048 replicated probes and 963 not replicated specific for the Ensembl (Ver. 56) Transcripts (protein coding + pseudogenes + retrotransposed elements), 11,363 replicated probes specific for the UniGene clusters (Ver. 38) of length comprised between 778 nt and 1,348 nt, and 28,790 single probes specific for the remaining UniGene clusters. These microarrays were used to study gene expression in 9 different pig tissues involved in the cardiocirculatory system (Left Atrium; Right Ventricle, Inferior Vena Cava, Superior Vena Cava, Ascending Aorta, Descending Aorta, Pulmonary Artery, Coronary Artery, Leaflet of Pulmonary Artery). Gene expression was correlated with the micro-RNA expression in the same tissues, also deposited at ArrayExpress under accession number E-MTAB-1938 (https://www.ebi.ac.uk/arrayexpress/experiments/E-MTAB-1938).
Project description:Pancreatic ductal adenocarcinoma (PDAC) cells undergo epithelial mesenchymal transdifferentiation (EMT) in adaption to environmental cues, including inflammation, a process that combines tumour cell dedifferentiation with dissemination and acquisition of stemness features. However, the mechanisms coupling inflammation-induced signalling pathways with EMT and stemness remain largely unknown. Here, we reveal the inflammation-induced transcription factor NFATc1 as a central regulator of pancreatic cancer cell plasticity.
Project description:Total RNA was extracted from liver tissues of lab-reared threespine stickleback. The dataset combines transcripts common to two experiments: first generation fish originating from the Baltic Sea near Helsinki (Finland) bred using a paternal half-sib design (E-MTAB-3098), and second generation fish originating from three different Fennoscandian populations bred from a full-sib design. Annotated R scripts defining the normalization procedures are available as additional files (see http://www.ebi.ac.uk/arrayexpress/files/E-MTAB-3099). Additional files also include a metadata file (matrix.df.csv) to facilitate construction of design matrices used by the snm package.
Project description:Transgenic mice were generated that expressed the inhibitor of apoptosis and mitotic regulator survivin in pancreatic islet beta cells. Control non-transgenic or transgenic islets were then used in a model of islet transplantation in diabetic recipient mice and tested for their ability to correct hyperglycemia and allow long-term engraftment of tranplanted islets in vivo. Control or transgenic islets were analyzed by chip microarray for potential transcriptional changes associated with transgenic expression of survivin, in vivo.
Project description:Background: Pachymic acid (PA) is a purified triterpene extracted from medicinal fungus Poria cocos. In this paper, we investigated the anticancer effects of PA on human chemotherapy resistant pancreatic cancer cells. Methods: Gemcitabine-resistant pancreatic cancer cells PANC-1 and MIA PaCa-2 were used, along with a xenograft model of MIA PaCa-2 cells implanted in mice. Apoptosis was assessed by quantitation of cytoplasmic histone-associated DNA fragments and expression of cleaved PARP. Differential expression of genes was identified using comparative DNA microarray analysis. Protein levels were determined by immunoblotting. Toxicology studies in vivo were assessed by detecting pathological changes in organs and liver enzyme profiles in plasma. Tumor tissues were analyzed by quantification of apoptotic bodies, qRT-PCR and immunoblotting. Principal Findings: PA induced endoplasmic reticulum (ER) stress in chemotherapy resistant pancreatic cancer cells through activation of heat shock response and unfolded protein response related genes, which further triggered apoptosis. The involvement of ER stress was confirmed by increasing expression of XBP-1s, ATF4, Hsp70, CHOP and phospho-eIF2M-NM-1. Moreover, 25 mg kgM-bM-^HM-^R1 of PA significantly suppressed MIA PaCa-2 tumor growth in vivo without toxicity, which correlated with induction of apoptosis, ER stress related genes and proteins expression. Conclusions: Growth inhibition and induction of apoptosis by PA in chemotherapy resistant pancreatic cancer cells were associated with ER stress activation both in vitro and in vivo. Pancreatic cancer cell line treated with pachymic acid vs. control (untreated)
Project description:Early invasive growth and metastasis are features of pancreatic cancer that rely on resistance to anoikis, an apoptosis program activated upon loss of adequate matrix anchorage. Re-expression of the tumor suppressor p16 reversed anoikis resistance of pancreatic cancer cells. This conversion to an anoikis-susceptible phenotype was found to be associated with a striking loss of GNE mRNA expression, prompting us to address the role of GNE in pancreatic cancer in more detail. GNE catalyzes a rate-limiting key step of the sialic acid biosynthesis and may have additional functions in the nucleus. Pancreatic cancer cells Capan-1. Three GNE-silencing samples and three control samples.
Project description:Early invasive growth and metastasis are features of pancreatic cancer that rely on resistance to anoikis, an apoptosis program activated upon loss of adequate matrix anchorage. Re-expression of the tumor suppressor p16 reversed anoikis resistance of pancreatic cancer cells. This conversion to an anoikis-susceptible phenotype was found to be associated with a striking loss of GNE mRNA expression, prompting us to address the role of GNE in pancreatic cancer in more detail. GNE catalyzes a rate-limiting key step of the sialic acid biosynthesis and may have additional functions in the nucleus. Pancreatic cancer cells Capan-1. Three p16-transfectants and three mock-transfectants.
Project description:Based on data-independent acquisition (DIA)-mass spectrometry (MS) proteomics, we first established a high-coverage human pancreatic cells spectrum library. Furthermore, analyzed the sensitivity and drug resistance phenotypes to gemcitabine (GEM).
Project description:Based on data-independent acquisition (DIA)-mass spectrometry (MS) strategies for in-depth proteome analysis, we established a high-coverage spectrum library from seven human pancreatic cell lines and evaluated performance of the library by exploring the molecular change between gemcitabine (GEM) sensitivity and resistance phenotypes .