Project description:We aim to determine blood transcriptome-based molecular signature of acute coronary syndrome (ACS), and to identify novel serum biomarkers for early stage ST-segment-elevation myocardial infarction (STEMI) We obtained peripheral blood from the patients with ACS who visited emergency department within 4 hours after the onset of chest pain: ST-elevation myocardial infarction (STEMI, n=7), Non-ST-elevation MI (NSTEMI, n=10) and unstable angina (UA, n=9), and normal control (n=7)
Project description:we assessed characteristic molecular and proteomic signatures in rat liver treated with drugs (pyrazinamide, ranitidine, enalapril, carbamazepine, and chlorpromazine) that are known to cause DILI in humans. In the present study, we assessed the characteristic gene expression signature for DILI in a rat model. Rats were administered representative drugs that are already known to induce DILI in humans and transcriptomic changes in rat liver were analyzed. The representative drugs, which induce three types (hepatocellular, mixed, and cholestatic) of DILI, that were used in this study were pyrazinamide (PZA, 150~1500 mg/kg), ranitidine (RAN, 209.5~2095 mg/kg), enalapril (ENA, 148.65~1486.5 mg/kg), carbamazepine (CBZ, 97.85~978.5 mg/kg), and chlorpromazine (CPZ, 7.1~71 mg/kg).
Project description:We aim to determine blood transcriptome-based molecular signature of acute coronary syndrome (ACS), and to identify novel serum biomarkers for early stage ST-segment-elevation myocardial infarction (STEMI) We obtained peripheral blood from the patients with ACS who visited emergency department within 4 hours after the onset of chest pain: a set of blood samples of patients with STEMI (n=7) before and 7 days after the primary percutaneous coronary intervention (n=7) and normal control (n=10)
Project description:Analysis of global gene expression after BRD4 inhibition by JQ1 in liver cancer cell lines SK-Hep1 Total RNA obtained from human liver cancer cell line SK-Hep1 cells after treatment of JQ1
Project description:To investigate the specific roles of HDAC6 in the development of liver cancer, we employed large-scale gene expression analysis to identify the molecular signature that may affect enabling characteristics of cancer cells. Differentially expressed genes were analyzed on the Hep3B cells transfected with empty mock or pcDNA_HDAC6, and recapitulated molecular signatures that related to hallmarks of cancer. To characterize the biological effects of HDAC6 on liver cancer, large-scale gene expression analysis to identify molecular signature was performed on the Hep3B cells.
Project description:To investigate the specific roles of HDAC2 in the development of liver cancer, we employed large-scale gene expression analysis to identify the molecular signature that may affect enabling characteristics of cancer cells. Differentially expressed genes were analyzed on the Hep3B cells transfected with HDAC2 shRNAs, and recapitulated molecular signatures that related to hallmarks of cancer. With the aim of identifying changes in gene expression following gene knockdown of HDAC2, we performed expression profiling in shRNA expression vector-transfected Hep3B cells, and compared the results to those obtained from vector-transfected Hep3B cells.
Project description:To investigate the specific roles of SIRT1 in the development of hepatocellular carcinoma, we employed large-scale gene expression analysis to identify the molecular signature that may affect enabling characteristics of cancer cells. Differentially expressed genes were analyzed on the SNU-182 cells transfected with SIRT1 siRNA and recapitulated molecular signatures that related to hallmarks of cancer. SIRT1 expression in hepatocellular carcinoma was analyzed by RT-PCR and western blot. RNA interference-mediated protein knockdown method was used to investigate oncogenic potential of SIRT1 in hepatocelluar carcinoma
Project description:To investigate the specific roles of SIRT7 in the development of HCC, we employed large-scale gene expression analysis to identify the molecular signature that may affect enabling characteristics of cancer cells. Differentially expressed genes were analyzed on the Hep3B cells transfected with SIRT7 shRNAs, and recapitulated molecular signatures that related to hallmarks of cancer. For each of the experimental conditions, total RNA was extracted from three independent sets of the corresponding cell lines using TRIzol Reagent (Invitrogen), followed by clean up on Ambion columns (Illumina Total-Prep RNA Amplification Kit, Ambion). For each experimental condition, an RNA pool was then obtained by mixing equal quantities of total RNA from each of the three independent RNA extractions. Biotin-labelled cRNA targets were synthesized starting from 1.5 µg of total RNA. Double stranded cDNA synthesis was performed with Illumina® TotalPrep RNA Amplification Kit (Ambion), and biotin-UTP-labelled antisense RNA was transcribed in vitro using Ambion’s Kit. All steps of the labelling protocol were performed as suggested by Ambion (http://www.ambion.com/techlib/prot/ fm_IL1791.pdf). The size and the accuracy of quantitation of targets were checked by Experion (Bio-rad Laboratories., Hercules, CA) electrophoresis system, prior to and after cRNA purification. After purification, targets were diluted in hybridization buffer at a concentration of 240 ng/µl, and hybridization was allowed to proceed at 58°C for 20 h. For microarray analysis, the Illumina HumanHT-12 v4 Sentrix Expression BeadChip was used (Illumina, San Diego, CA). Hybridization of labelled cRNA to the BeadChip, washing, and scanning were performed according to the Illumina BeadStation 500× manual. The array signal was developed via 10-min incubation with streptavidin-Cy3. The HumanHT-12 v4 Sentrix Expression BeadChip was washed and subsequently dried via centrifugation for 4 min at a setting of 275 xg. The arrays were scanned on the Illumina BeadArray reader, a confocal-type imaging system with 532 (Cy3) nm laser illumination. Data from each sample was extracted with Genome Studio software (Illumina) using default parameters and then analyzed using GenPlex 3.0.
Project description:HDAC1 aberrantly over expressed in HCC and it was considered as an oncogene gene in HCC development. So we want to analyze in greater detail of the genes regulated by HDAC1 using microarray assay. Hep3B RNA was extracted after transfected by HDAC1 shRNA or scrambled shRNA (Mock) for 72hr. For microarray analysis of gene expression unpon depletion of HDAC1, 0.5 μg of total RNA was used to make biotin-labeled cRNA using the Ambion Illumina cRNA amplification and labeling kit according to manufacturers’ instructions (Ambion, Austin, TX)
Project description:To investigate the specific roles of HDAC2 in the development of gastric cancer, we employed large-scale gene expression analysis to identify the molecular signature that may affect enabling characteristics of cancer cells. Differentially expressed genes were analyzed on the MKN-1 cells transfected with HDAC2 shRNAs, and recapitulated molecular signatures that related to hallmarks of cancer. DNA methylation of p16INK4a promoter region was assessed by methylation specific polymerase chain reaction. Recruiting the HDAC2 at the p16INK4a promoter was identified using chromatin immunoprecipitation assay. RNA interference-mediated protein knockdown method was used to investigate oncogenic potential of HDAC2 in in vitro and in vivo gastrocarcinogenesis of MKN-1 cells. RNA interference-mediated protein knockdown versus mock treatment