Project description:Gene expression profiling of pancreatic cancer cell PANC-1 and SW1990 when LINC00842 knockdown by CRISPR/Cas9 system. We identified LINC00842 is a novel prognosis related lincRNA in pancreatic cancer and its regulation networks is poorly understood. We used the total RNA from knockdown control and LINC00842-knockdown PANC-1 and SW1990 cells to analyze the differentially expressed genes which were regulated by LINC00842, and further explored the biological processes that LINC00842 may involved.
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
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: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: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: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
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:Serine/threonine/tyrosine kinase 1 (STYK1), a proto-oncogenic transmembrane receptor alternatively termed NOK which consists of a kinase domain, intracellular domain, and transmembrane domain, was identified as an oncogene with high transformation potential in multiple cancer types. Recently, our group recognized that STYK1 depletion disrupts autophagosome biogenesis, establishing it as a critical modulator of autophagic flux. STYK1 was also reported as an oncogenic amplifier that hijacks KRAS effector networks, specifically the PI3K/AKT and MEK/ERK signaling axes, to drive tumor progression across malignancies. This molecular paradigm gains particular relevance in PDAC, where somatic KRAS mutations dominate (~95% prevalence) and functionally orchestrate pancreatic carcinogenesis from its earliest premalignant stages, notably during pancreatic intraepithelial neoplasia (PanIN) precursor lesions. This prompted a focused investigation into STYK1's functional implications within pancreatic cancer. By using multiple in vitro and in vivo assays, we figured out that higher STYK1 expression is related to poor pancreatic cancer survival and that STYK1 depletion suppresses pancreatic cancer cell development.To determine the molecular mechanism by which STYK1 promotes pancreatic cancer development, we performed RNA sequencing and found that STYK1 is involved in regulating the Wnt/β-Catenin signaling pathway. We also elucidate a novel STYK1-driven mechanism for Wnt/β-catenin activation in APC-independent pancreatic cancer and provide preclinical evidence for targeting STYK1-mediated signaling as a therapeutic strategy.
Project description:Pancreatic cancer is a lethal diease with high tendency of metastasis. Howerver, the mechanisms of pancreatic cancer are sitill unclear. To explore the roles of N4-acetylation (ac4C) RNA modification and its involved N-Acetyltransferase 10 (NAT10) in pancreatic ductal adenocarcinoma (PDAC), we performed profiling by high throughput sequencing. In this study, we investigate the effects of NAT10 knockdown on N4-acetylcytidine (ac4C) modification in mRNA within PANC-1 cells using ac4C-seq. By employing RNA interference to specifically knock down NAT10 expression in PANC-1 cells, we aim to elucidate its impact on ac4C RNA modifications, which have been implicated in various cellular processes and cancer progression. Total RNA was extracted and mRNA was captured and treated with sodium borohydride (NaBH4) for detection of ac4C sites.Following library preparation, sequencing was performed on an Illumina Novaseq 6000 platform. Bioinformatics analyses identified significant changes in ac4C modification patterns due to NAT10 depletion. This dataset provides a valuable resource for further exploration of ac4C modifications in mRNA and their role in PDAC.