Project description:PANC-1Tet/ZIC2 and PANC-1Tet/empty were established from human pancreatic cancer cell line PANC-1. PANC-1Tet/ZIC2 cells express FLAG-tagged human ZIC2 on the withdrawal of DOX. On the other hand, PANC-1Tet/empty was transfected an empty vector for the control experiment. To identify ZIC2 target genes, total RNAs were purified from the cells before and 48 hours after the DOX withdrawal. Gene expression profiles were analyzed by AGILENT human 4x44k cDNA microarray. As well as ZIC2-inducible system, we performed ZIC2-knockdown experiments in PANC-1 human pancreatic cancer cells. After 96 hours transfection of siRNAs for ZIC2 and its control, total RNAs were purified and gene expression profiles were analyzed by AGILENT human 4x44k cDNA microarray. ZIC2 target genes were identified in PANC-1 cells. Gene expression profiles of PANC-1Tet/ZIC2 and PANC-1Tet/empty cells were analyzed by AGILENT human 4x44k cDNA microarray before and 48 hours after the DOX withdrawal. As well as ZIC2-inducible system, gene expression profiles of control- and ZIC2-knocdown PANC-1 cells were also analyzed by AGILENT human 4x44k cDNA microarray.
Project description:PANC-1Tet/ZIC2 and PANC-1Tet/empty were established from human pancreatic cancer cell line PANC-1. PANC-1Tet/ZIC2 cells express FLAG-tagged human ZIC2 on the withdrawal of DOX. On the other hand, PANC-1Tet/empty was transfected an empty vector for the control experiment. To identify ZIC2 target genes, total RNAs were purified from the cells before and 48 hours after the DOX withdrawal. Gene expression profiles were analyzed by AGILENT human 4x44k cDNA microarray. As well as ZIC2-inducible system, we performed ZIC2-knockdown experiments in PANC-1 human pancreatic cancer cells. After 96 hours transfection of siRNAs for ZIC2 and its control, total RNAs were purified and gene expression profiles were analyzed by AGILENT human 4x44k cDNA microarray.
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.
Project description:Analysis of differentially expressing genes in whole genome wide analysis of ALPPL2 expressing Panc-1 cells (Panc-1+ve) via siRNA mediated knockdown of ALPPL2 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 four chip study using total RNA recovered from Panc-1+ve cells transfected with siALPPL2-2, siALPPL2-3, siGFP control and Lipofectamine 2000 treatament . Each chip measures 45,033 genes with three 60 mer probe pairs per target.
Project description:Panc-1GLI1ER and Panc-1ER were established from human pancreatic cancer cell line Panc-1. Panc-1GLI1ER cells express a chimeric transgene composed of an enhanced green fluorescent protein (EGFP)-tagged version of the amino-terminal half of GLI1, fused to the AF2 domain of the mouse estrogen receptor 1(Esr1) cDNA. On the other hand, Panc-1ER harbor only EGFP-tagged AF2 domain. To identify GLI1 direct target genes, total RNAs were purified from the cells before and 3 hours after the beta-estradiol (E2) treatment. Gene expression profiles were analyzed by AGILENT human 4x44 cDNA microarray. Keywords: Expression profiling by genome tiling array GLI1 direct target genes were identified in Panc-1 cells. Gene expression profiles of Panc-1GLI1ER and Panc-1ER cells were analyzed by AGILENT human 4x44 cDNA microarray before and 3 hours after treatment of beta-estradiol (E2) at doses of 10nM.
Project description:To explore malignant phenotype related genes in Panc-1-CTC, we performed gene expression array analysis with Panc-1-CTC and Panc-1-Parent (Panc-1-P). As a result, TGFBI upregulation emerged as highly malignant feature for pancreatic ductal adenocarcinoma. Identification of malignant phenotype related genes in pancreatic ductal adenocarcinoma
Project description:The Cancer associated Sm-like (CaSm) oncogene is overexpressed in 87% of human pancreatic tumor samples and CaSm knockdown has demonstrated therapeutic efficacy in murine models of pancreatic cancer. Evidence indicates that CaSm modulates mRNA degradation; however, its target genes and the mechanisms by which CaSm promotes pancreatic cancer remain largely unknown. Here, we demonstrate that the CaSm overexpression alters several hallmarks of cancer – including transformation, proliferation, chemoresistance, and metastasis. Doxycycline-induced CaSm expression enhanced proliferation and both anchorage-dependent and -independent growth of the human Panc-1 cells in vitro. CaSm induction decreased gemcitabine-induced cytotoxicity and altered the expression of apoptotic regulation genes, including Bad, E2F1, and Bcl-XL. CaSm-overexpressing Panc-1 cells were 2-fold more migratory and 4-fold more invasive than the driver controls and demonstrated characteristics of epithelial-to-mesenchymal transition such as morphological changes and decreased E-cadherin expression. CaSm induction resulted in changes in RNA expression of metastasis-associated genes such as MMP1, SerpinB5, uPAR, and Slug. Using a murine model of metastatic pancreatic cancer, injection of CaSm-induced Panc-1 cells resulted in a higher abundance of hepatic metastatic lesions. Overall, CaSm overexpression contributed to a more aggressive cancer phenotype in Panc-1 cells, further supporting the use of CaSm as a therapeutic target against pancreatic cancer.
Project description:To identify differentially expressed genes by anti cancer treatments (microRNAs or siRNAs) in human cancer, several cell lines (pancreatic cancer, hypopharyngeal squamous cell carcinoma and prostate cancer) were subjected to Agilent whole genome microarrays. Human cell lines (Panc-1, FaDu and PC3) were treated with miRNAs (miR99a-5p, miR-99a-3p, miR-100-3p, miR-150-5p and miR-150-3p), siRNAs (si-FOXQ1).