RNA-Seq of pancreatic cancer cell line CAPAN-2 with or without SIRT4 overexpression
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE201110 | GEO | 2022/05/31
REPOSITORIES: GEO
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Project description:RNA-Seq of pancreatic cancer cell line CAPAN-2 with or without SIRT4 overexpression
| PRJNA828435 | ENA
Project description:Sirtuins are a family of protein deacetylases, deacylases, and ADP-ribosyltransferases that regulate life span, control the onset of numerous age-associated diseases, and mediate metabolic homeostasis. We have uncovered a novel role for the mitochondrial sirtuin SIRT4 in the regulation of hepatic lipid metabolism during changes in nutrient availability. We show that SIRT4 levels decrease in the liver during fasting and that SIRT4 null mice display increased expression of hepatic peroxisome proliferator activated receptor (PPAR ) target genes associated with fatty acid catabolism. Accordingly, primary hepatocytes from SIRT4 knockout (KO) mice exhibit higher rates of fatty acid oxidation than wild-type hepatocytes, and SIRT4 overexpression decreases fatty acid oxidation rates. The enhanced fatty acid oxidation observed in SIRT4 KO hepatocytes requires functional SIRT1, demonstrating a clear cross talk between mitochondrial and nuclear sirtuins. Thus, SIRT4 is a new component of mitochondrial signaling in the liver and functions as an important regulator of lipid metabolism. SIRT4 knockout (KO) and wild-type (WT) littermates (male; n 6 per genotype; 7- to 8-month-old littermates) were sacrificed after a 16-h overnight fast. Samples were individually hybridized on Affymetrix Mouse Genome 430 2.0 GeneChips by the Biopolymers Facility (Harvard Medical School).
2014-03-28 | E-GEOD-56321 | biostudies-arrayexpress
Project description:Sirtuins are a family of protein deacetylases, deacylases, and ADP-ribosyltransferases that regulate life span, control the onset of numerous age-associated diseases, and mediate metabolic homeostasis. We have uncovered a novel role for the mitochondrial sirtuin SIRT4 in the regulation of hepatic lipid metabolism during changes in nutrient availability. We show that SIRT4 levels decrease in the liver during fasting and that SIRT4 null mice display increased expression of hepatic peroxisome proliferator activated receptor (PPAR ) target genes associated with fatty acid catabolism. Accordingly, primary hepatocytes from SIRT4 knockout (KO) mice exhibit higher rates of fatty acid oxidation than wild-type hepatocytes, and SIRT4 overexpression decreases fatty acid oxidation rates. The enhanced fatty acid oxidation observed in SIRT4 KO hepatocytes requires functional SIRT1, demonstrating a clear cross talk between mitochondrial and nuclear sirtuins. Thus, SIRT4 is a new component of mitochondrial signaling in the liver and functions as an important regulator of lipid metabolism.
2014-03-28 | GSE56321 | GEO
Project description:Paeoniflorin (PF) is an active monoterpene glycoside extracted from Paeonia lactiflora Pall. Recent studies showed that PF has anti-tumor effects in various types of cancer. However, the function of PF in pancreatic cancer (PA) is largely unexplored. Here, we showed that PF suppressed growth of PA cell lines Capan-1 and MIAPaCa-2, and profoundly sensitized these cells to X-ray irradiation. Through a microarray analysis, we identified tumor-suppressor candidate gene HTRA3 as the most increased gene upon PF treatment in Capan-1 cells. Ectopic expression of HTRA3 led to reduced cell growth and increased expression of apoptotic protein Bax, suggesting a tumor suppressive role of HTRA3 in PA cells. Together, our results provide a set of genetic and biologic proofs that PF inhibited PA cell growth by upregulation of HTRA3.
2017-09-20 | GSE97124 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE22334: Induction of apoptotic processes in Capan-1 pancreatic carcinoma cells by restoration of p16INK4a expression GSE22336: UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE) is an inducer of apoptotic processes in Capan-1 pancreatic carcinoma cells: GNE silencing Refer to individual Series
2010-08-01 | E-GEOD-22337 | biostudies-arrayexpress
Project description:Analysis of differentially expressing genes in whole genome wide analysis of aptamer SQ2 positive cells (Capan-1, Panc-1, Panc-1+ve) and SQ2 negative cells (Panc-1-ve and HPDE) Panc-1 +ve and Panc-1-ve cell lines were generated from Panc-1 cell line based upon its hetergenous binding to aptamer SQ2. Detailed procedure of generation of these cell lines are described in Pooja Dua, Hye Suk Kang, Seung-Mo Hong, Ming-Sound Tsao, Soyoun Kim, and Dong-ki Lee. 2012 Alkaline Phosphatase ALPPL2 is a novel pancreatic carcinoma-associated protein. Cancer Research A five chip study using total RNA recovered from Capan-1, Panc-1, Panc-1+ve, Panc-1-ve and HPDE cells. Each chip measures 45,033 genes with three 60 mer probe pairs per target.
2012-11-21 | E-GEOD-42428 | biostudies-arrayexpress
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.
2010-08-01 | E-GEOD-22334 | biostudies-arrayexpress
Project description:Analysis of differentially expressing genes in whole genome wide analysis of aptamer SQ2 positive cells (Capan-1, Panc-1, Panc-1+ve) and SQ2 negative cells (Panc-1-ve and HPDE) Panc-1 +ve and Panc-1-ve cell lines were generated from Panc-1 cell line based upon its hetergenous binding to aptamer SQ2. Detailed procedure of generation of these cell lines are described in Pooja Dua, Hye Suk Kang, Seung-Mo Hong, Ming-Sound Tsao, Soyoun Kim, and Dong-ki Lee. 2012 Alkaline Phosphatase ALPPL2 is a novel pancreatic carcinoma-associated protein. Cancer Research
2012-11-21 | GSE42428 | GEO
Project description:Pancreatic cancer cells are inherently highly resistant to spontaneous or chemotherapy-induced apoptosis. The human pancreatic tumor cell line Capan-1 (pRB+/p16-) was stably transfected with p16 expression constructs or control plasmids to functionally inactivate pRB. Three independent experiments were conducted
2015-02-27 | E-MTAB-3370 | biostudies-arrayexpress
Project description:Sirtuins are deacetylases or ADP-ribosyltransferases which are implicated in multiple pathways involved in metabolism and life-span regulation. Here, we link the mitochondrial sirtuin SIRT4, which overexpression negatively impacts on mitochondrial oxidative capacity, with premature senescence and skin aging. Accordingly, SIRT4 mRNA levels were significantly increased in vitro in human dermal fibroblasts after repetitive UVB exposure or in senescence triggered by mitotic spindle stress or ionizing radiation. Similarly, analysis of SIRT4 expression in vivo in human skin revealed upregulation of SIRT4 mRNA levels in the dermal compartment of photaged skin as compared with the dermis of intrinsically aged skin. In all our in vitro models, upregulation of SIRT4 expression was associated with decreased levels of miR-15b. Also, in human skin, highest copy numbers of miR-15b mRNA were detected in the epidermis, and epidermal expression was significantly reduced in photoaged skin as compared with intrinsically aged skin. Reduced miR-15b expression is most likely causally linked to increased SIRT4 expression because we found that (i) miR-15b displays a conserved and direct binding site within the 3'-untranslated region of the SIRT4 gene as demonstrated by luciferase reporter assays and (ii) transfection of oligonucleotides mimicking miR-15b function was sufficient to prevent SIRT4 upregulation in senescent cells in vitro. Thus, we propose that miR-15b acts as a negative regulator of SIRT4 expression to antagonize mitochondrial dysfunction and hence cellular senescence as well as tissue aging, in particular photoaging of the skin.
2016-06-08 | GSE45729 | GEO