Neuroblastoma tumors with favorable and unfavorable outcomes: Significant differences in mRNA expression of genes mapped at 1p36.2

2006 ◽  
Vol 46 (1) ◽  
pp. 45-52 ◽  
Author(s):  
Susanne Fransson ◽  
Tommy Martinsson ◽  
Katarina Ejeskär
Keyword(s):  
Mrna Expression ◽  
Expression Of Genes

8712 POSTER Validation of Differential mRNA Expression of Genes in Astrocytoma

2011 ◽  
Vol 47 ◽  
pp. S578
Author(s):  
C. Diez-Tascón ◽  
A. de la Hera ◽  
O. Rivero-Lezcano ◽  
L. Vilorio ◽  
E. Santin ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Expression Of Genes ◽  
Differential Mrna Expression

Abstract 191: NF-?B p65 Methylation by Protein Arginine Methyltransferase 5 (PRMT5) is Necessary for the Transcriptional Induction of CXCL10 by TNF-a

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Daniel P Harris
Keyword(s):  
Endothelial Cells ◽  
Mrna Expression ◽  
Chromatin Immunoprecipitation ◽  
Proximal Promoter ◽  
Protein Arginine Methyltransferase ◽  
Arginine Methyltransferase ◽  
Expression Of Genes ◽  
Tnf Α ◽  
Affect Expression ◽  
Transcriptional Induction

TNF-α initiates the expression of genes involved in the recruitment, adhesion, and transmigration of leukocytes to sites of inflammation. Here, we report that the protein arginine methyltransferase PRMT5 is required for the transcriptional induction of the pro-inflammatory chemokine CXCL10 (IP-10) in endothelial cells. Depletion of PRMT5 by siRNA results in significantly diminished TNF-α-induced CXCL10 mRNA expression, but does not affect expression of other chemokines, such as MCP-1 or IL-8. Chromatin immunoprecipitation experiments of the CXCL10 proximal promoter show the presence of symmetrical dimethylated arginine (sDMA)-containing proteins upon exposure to TNF-α. This methylation is completely lost when PRMT5 is removed from cells by siRNA. Using immunoprecipitation, we show that PRMT5 enhances CXCL10 expression by methylating the RelA (p65) subunit of NF-κB. In summary, we have identified that PRMT5 is a novel regulator of CXCL10 expression. Further, we have discovered that PRMT5 methylates NF-κB, a finding which may further knowledge of the post-translational code governing NF-κB regulation and target specificity.

Effects of lipotoxicity on a novel insulin-secreting human pancreatic β-cell line, 1.1B4

2013 ◽  
Vol 394 (7) ◽  
pp. 909-918 ◽  
Author(s):  
Srividya Vasu ◽  
Neville H. McClenaghan ◽  
Jane T. McCluskey ◽  
Peter R. Flatt
Keyword(s):  
Mrna Expression ◽  
Cell Line ◽  
Molecular Mechanisms ◽  
Endoplasmic Reticulum Stress Response ◽  
Future Research ◽  
The Novel ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Expression Of Genes ◽  
Cellular Ca

Abstract The novel insulin-secreting human pancreatic β-cell line, 1.1B4, demonstrates stability in culture and many of the secretory functional attributes of human pancreatic β-cells. This study investigated the cellular responses of 1.1B4 cells to lipotoxicity. Chronic 18-h exposure of 1.1B4 cells to 0.5 mm palmitate resulted in decreased cell viability and insulin content. Secretory responses to classical insulinotropic agents and cellular Ca2+ handling were also impaired. Palmitate decreased glucokinase activity and mRNA expression of genes involved in secretory function but up-regulated mRNA expression of HSPA5, EIF2A, and EIF2AK3, implicating activation of the endoplasmic reticulum stress response. Palmitate also induced DNA damage and apoptosis of 1.1B4 cells. These responses were accompanied by increased gene expression of the antioxidant enzymes SOD1, SOD2, CAT and GPX1. This study details molecular mechanisms underlying lipotoxicity in 1.1B4 cells and indicates the potential value of the novel β-cell line for future research.

scholarly journals Short communication: Colostrum versus formula: Effects on mRNA expression of genes related to branched-chain amino acid metabolism in neonatal dairy calves

2020 ◽  
Vol 103 (10) ◽  
pp. 9656-9666 ◽  
Author(s):  
Morteza H. Ghaffari ◽  
Hassan Sadri ◽  
Harald M. Hammon ◽  
Julia Steinhoff-Wagner ◽  
Nico Henschel ◽  
...  
Keyword(s):  
Amino Acid ◽  
Mrna Expression ◽  
Amino Acid Metabolism ◽  
Short Communication ◽  
Acid Metabolism ◽  
Dairy Calves ◽  
Branched Chain Amino Acid ◽  
Expression Of Genes ◽  
Branched Chain

Characterization of mRNA Expression of Genes Involved in Megakaryocyte Development in Higher-Risk Myelodysplastic Syndromes

2017 ◽  
Vol 55 ◽  
pp. S99
Author(s):  
E. Fabiani ◽  
G. Falconi ◽  
M. Criscuolo ◽  
L. Fianchi ◽  
A. Picardi ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Myelodysplastic Syndromes ◽  
Expression Of Genes

Proteasome Inhibitors and a Fusicoccin Derivative (ISIR-042) Cooperatively Inhibit Proliferation of Myeloma Cells through Induction of C/EBP-Homologous Protein (CHOP/GADD153)

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 5657-5657
Author(s):  
Takaaki Miyake ◽  
Yoshio Honma ◽  
Tsutomu Takahashi ◽  
Koshi Kawakami ◽  
Takahiro Okada ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Mrna Expression ◽  
Research Funding ◽  
Synergistic Effects ◽  
Proteasome Inhibitors ◽  
Cytotoxic Effects ◽  
Myeloma Cells ◽  
Expression Of Genes ◽  
Genes Encoding ◽  
Human Multiple Myeloma

Abstract Combinations of bortezomib and novel targeted therapeutic agents may synergistically increase antitumor effect and may overcome specific cellular resistance and/or antiapoptotic processes. However, highly effective combinations of bortezomib with targeted therapeutic agents have not been developed to date. We examined the synergistic effects of various compounds and bortezomib on myeloma cells and identified fusicoccin derivative ISIR-042 as the most potent drug. We developed ISIR-042 that exerts higher cytotoxic effects on hypoxic cells than on normoxic cells and that preferentially inhibits stem/progenitor cells in pancreatic cancer cell lines compared with other chemotherapeutic agents (Kawakami et al, Anticancer Agents Med Chem 2012). In the present study, we determined the synergistic effects of bortezomib and ISIR-042 cotreatment on human multiple myeloma cells. Human multiple myeloma cell lines RPMI8226, KMS-11, and KMS-26 were cultured in RPMI-1640 supplemented with 10% fetal bovine serum (FBS) at 37°C in a humidified atmosphere of 5% CO2 in air. Viability of cells cultured with or without the test compounds for indicated time was examined by performing a modified MTT assay.Bone marrow specimens and ascitic fluids were collected from patients at diagnosis or relapse after obtaining written informed consent for sample collection in accordance with institutional policy. The study was approved by the Institutional Review Board of Shimane University. For performing colony-forming assay, the cells (1 × 104/dish) were plated in 1.1 ml semisolid methylcellulose medium supplemented with 0.8% methylcellulose and 20% FBS in triplicates for 10 days. CHOP-/- and CHOP+/+ MEF cells were maintained in Dulbecco's modified Eagle's medium supplemented with 10% FBS. Expression of cell surface antigens was analyzed by performing flow cytometry with anti-CD38 or anti-CD138 antibody. Combined effects of myeloma cells in primary culture were analyzed by performing flow cytometry with anti-CD19 and anti-CD138 antibodies. Expression of caspase-10, BCL-2, p62, BCLAF1, LC3, actin, and CHOP was determined by performing western blotting with respective monoclonal antibodies. mRNA expression of genes encoding XBP-1u and XBP-1s was analyzed by performing reverse transcription-PCR. CHOP mRNA levels were measured by performing real-time PCR. ISIR-042 inhibited the growth of RPMI8226 cells in a concentration-dependent manner and exerted synergistic effects with bortezomib. ISIR-042 also exerted synergistic effects with carfilzomib. Results of flow cytometry showed that the combination of ISIR-042 and bortezomib decreased the number of myeloma cells in the primary culture in a concentration-dependently. Colony-forming assay showed that RPMI8226 cells were more sensitive than normal mouse hematopoietic cells to ISIR-042 and bortezomib cotreatment. ISIR-042 decreased the number of CD38-CD138- cells and increased the number of CD38+CD138+ cells in KMS11 cell population. mRNA expression of genes encoding XBP-1u and XBP-1s was not affected in RPMI8226 cells treated with ISIR-042 or bortezomib alone. However, mRNA expression of the gene encoding XBP-1s significantly increased in RPMI8226 cells cotreated with ISIR-042 and bortezomib. Growth-inhibitory effects of ISIR-042 and bortezomib were not associated with caspase-10 which modulates autophagic response for survival. Expression of autophagic markers such as LC3 and p62 was also examined. ISIR-042 exerted modest effects in the presence or absence of bortezomib. ER stress-mediated CHOP induction promotes the cytotoxic effects of proteasome inhibitors on many cancer cells. Carfilzomib and ISIR-042 cotreatment significantly induced CHOP mRNA expression, suggesting that ISIR-042 and proteasome inhibitor cotreatment induced apoptosis by enhancing ER stress and activating CHOP. This was confirmed using CHOP-/- MEF cells. Our results showed that carfilzomib and ISIR-042 cotreatment did not exert cytotoxic effects on CHOP-/- MEF cells. These results suggest that treatment of multiple myelomas with ISIR-042-supplemented proteasome inhibitor-based chemotherapy exerts beneficial anticancer effects. Disclosures Suzuki: Chugai: Honoraria; Bristol-Myers Squibb: Honoraria; Kyowa Hakko kirin: Honoraria. Suzumiya:Astellas: Research Funding; Takeda: Honoraria; Eisai: Honoraria, Research Funding; Kyowa Hakko kirin: Research Funding; Chugai: Honoraria, Research Funding; Toyama Chemical: Research Funding.

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