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KSN01_Proteome_CellLine: Aberrant (pro)renin receptor expression induces genomic instability in pancreatic ductal adenocarcinoma through upregulation of SMARCA5/SNF2H

ABSTRACT: Aberrant (pro)renin receptor expression induces genomic instability in pancreatic ductal adenocarcinoma through upregulation of SMARCA5/SNF2H

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Akira Nishiyama

PROVIDER: PXD010107 | JPOST Repository | Tue Dec 15 00:00:00 GMT 2020

REPOSITORIES: jPOST

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			Action	DRS
	20170630_58_Kagawa_cont_1_5uL.raw	Raw
	20170630_62_Kagawa_cont_2_5uL.raw	Raw
	20170630_66_Kagawa_cont_3_5uL.raw	Raw
	20170630_70_Kagawa_cont_4_5uL.raw	Raw
	20170630_74_Kagawa_cont_5_5uL.raw	Raw

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Publications

Aberrant (pro)renin receptor expression induces genomic instability in pancreatic ductal adenocarcinoma through upregulation of SMARCA5/SNF2H.

Shibayama Yuki Y Takahashi Kazuo K Yamaguchi Hisateru H Yasuda Jun J Yamazaki Daisuke D Rahman Asadur A Fujimori Takayuki T Fujisawa Yoshihide Y Takai Shinji S Furukawa Toru T Nakagawa Tsutomu T Ohsaki Hiroyuki H Kobara Hideki H Wong Jing Hao JH Masaki Tsutomu T Yuzawa Yukio Y Kiyomoto Hideyasu H Yachida Shinichi S Fujimoto Akihiro A Nishiyama Akira A

Communications biology 20201127 1

(Pro)renin receptor [(P)RR] has a role in various diseases, such as cardiovascular and renal disorders and cancer. Aberrant (P)RR expression is prevalent in pancreatic ductal adenocarcinoma (PDAC) which is the most common pancreatic cancer. Here we show whether aberrant expression of (P)RR directly leads to genomic instability in human pancreatic ductal epithelial (HPDE) cells. (P)RR-expressing HPDE cells show obvious cellular atypia. Whole genome sequencing reveals that aberrant (P)RR expressio ...[more]

PMID: 33247206

Similar Datasets

Aberrant (pro)renin receptor expression induces genomic instability in pancreatic ductal adenocarcinoma through upregulation of SMARCA5/SNF2H.

Project description:(Pro)renin receptor [(P)RR] has a role in various diseases, such as cardiovascular and renal disorders and cancer. Aberrant (P)RR expression is prevalent in pancreatic ductal adenocarcinoma (PDAC) which is the most common pancreatic cancer. Here we show whether aberrant expression of (P)RR directly leads to genomic instability in human pancreatic ductal epithelial (HPDE) cells. (P)RR-expressing HPDE cells show obvious cellular atypia. Whole genome sequencing reveals that aberrant (P)RR expression induces large numbers of point mutations and structural variations at the genome level. A (P)RR-expressing cell population exhibits tumour-forming ability, showing both atypical nuclei characterised by distinctive nuclear bodies and chromosomal abnormalities. (P)RR overexpression upregulates SWItch/Sucrose Non-Fermentable (SWI/SNF)-related, matrix-associated, actin-dependent regulator of chromatin, subfamily a, member 5 (SMARCA5) through a direct molecular interaction, which results in the failure of several genomic stability pathways. These data reveal that aberrant (P)RR expression contributes to the early carcinogenesis of PDAC.

| S-EPMC7695732 | biostudies-literature

Upregulation of FOXM1 Induces Genomic Instability in Human Epidermal Keratinocytes

Project description:Genome-wide 10k SNP profiling of FOXM1B-transduced N/TERT and primary normal human epidermal keratinocytes (NHEK). The aim of this study was to study the cancer initiation role of UVB and FOXM1B upregulation in NHEK. Upregulation of FOXM1B alone (without UVB) was found to directly induce genomic instability in the form of copy number aberration (CNA) and low levels of loss of heterozygosity (LOH) in primary NHEK. The FOXM1B-induced CNA was found to be retained and accumulated in subsequent cell culture passages. UVB-exposure resulted in significant chromosomal LOH and CNA in N/TERT cells expressing FOXM1B but not in EGFP-expressing cells. This indicates that UVB corroborated with FOXM1B to recruit LOH and CNA which may predispose cell to malignant transformation. Collectively, these results indicate that aberrant upregulation of FOXM1B in skin keratinocytes following UVB exposure may be an early mechanism whereby cells acquire genomic changes required for oncogenesis. Keywords: Genome-wide SNP profiling for loss of heterozygosity (LOH) and copy number aberration (CNA), FOXM1, UVB, Keratinocytes, Basal cell carcinoma, genomic instability, carcinogenesis, squamous cell carcinoma. 1) Three individual normal primary NHEK cultures were retrovirally transduced (with either EGFP or EGFP-FOXM1B) and left to grow for 4 days prior to SNP array analysis. 2) EGFP or EGFP-FOXM1B-tansduced NHEK cells were harvested at passage 1, 2 and 3 for SNP array analysis to investigate if genomic instability is maintained and accumulated in subsequent passages. 3) N/TERT cells transduced with either EGFP or EFOX were UVB-irradiated and left to grow for 50 days in culture prior to SNP array analysis.

2010-07-29 | E-GEOD-16937 | biostudies-arrayexpress

Upregulation of FOXM1 Induces Genomic Instability in Human Epidermal Keratinocytes

2010-06-28 | GSE16937 | GEO

Pancreatic ductal adenocarcinoma

Project description:Pancreatic ductal adenocarcinoma

| PRJNA432344 | ENA

Identification of malignant phenotype related genes in pancreatic ductal adenocarcinoma

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

2018-08-24 | GSE118556 | GEO

Aberrant APOBEC3C expression induces characteristic genomic instability in pancreatic ductal adenocarcinoma.

Project description:Pancreatic ductal adenocarcinoma (PDAC) is a well-known lethal and heterogeneous disease. Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like (APOBEC) is an important mutagenic driver that has seldom been investigated in PDAC. Therefore, this study investigated the significance of APOBEC3C in PDAC. First, cytosine deamination-associated mutation signatures were identified in the PDAC cohorts from TCGA and Fudan University Shanghai Cancer Center (FUSCC) datasets, and C > X-enriched kataegis regions were identified in the FUSCC cohort (12 to 27 counts per sample). Patients were stratified according to APOBEC3C expression, and high APOBEC3C expression was found to correlate with a higher motif enrichment score of 5'-CC-3' and an elevated kataegis count within PCSK5 and NES genes. Second, we compared APOBEC expression in PDAC and normal pancreatic tissues and found that APOBEC3C was substantially upregulated in PDAC. APOBEC3C-overexpressing cell lines were generated to substantiate the effects of APOBEC3C on PDAC genome, including alterations in single-nucleotide variant (SNV) classes (higher proportion of C > T conversions) and the formation of kataegis regions (newly occurring kataegis regions detected in ACHE and MUC6 genes). Three different PDAC cohorts (FUSCC, TCGA, and QCMG) were analysed to evaluate the prognostic value of APOBEC3C, and APOBEC3C overexpression predicted shorter survival. Finally, the APOBEC3C overexpression correalted with the PDAC tumour microenvironment (TME) remodelling, APOBEC3C expression was associated with the invasion of CD4 + T lymphocytes and CD8 + T lymphocytes (cytotoxic T lymphocytes, CTLs), indicating enhanced immune activity and validating the practicality of APOBEC3C for guiding immunotherapy.

| S-EPMC9232547 | biostudies-literature

Genome profiling of pancreatic adenocarcinoma

Project description:Pancreatic adenocarcinoma is one of the most aggressive human cancers and displays many different chromosomal abnormalities and mutations. By using 244K high-resolution array-comparative genomic hybridization (aCGH) we studied the genome alterations of 39 fine-needle aspirations from pancreatic adenocarcinoma and 9 human adenocarcinoma pancreatic cell lines.

2011-12-31 | E-MTAB-570 | biostudies-arrayexpress

Pharmacologic activation of G protein-coupled estrogen receptor inhibits pancreatic ductal adenocarcinoma

Project description:We examine the effect of GPER activation on murine pancreatic ductal adenocarcinoma cell lines

2018-10-18 | GSE117312 | GEO

Transcriptional profiling by array of pancreatic ductal adenocarcinoma xenograft models

Project description:We generated novel patient derived xenograft (PDX) and cell line -derived xenograft models for pancreatic ductal adenocarcinoma (PDAC) which reflect different molecular subtypes. Pancreatic ductal adenocarcinoma is currently the tumor with the fourth highest mortality rate. Recently, subtypes of PDAC have been reported by Collisson et al (Nat. Med. 17(4) 2011. DOI: 10.1038/nm.2344). However current fetal calf serum (FCS) cultured cell lines do not accurately model these subtypes. We thus generated novel serum-free cell lines derived from primary patient xenografts. We here analyse the gene-expression profiles of the xenografts and the derived cell lines. We show that indeed three different subtypes can be separated in our models based on gene-expression data. Further, we identify upregulation of a drug-detoxification pathway specifically in xenografts and cell lines of one of the subtypes. These models and data will help to better understand inter-patient heterogeneity in PDAC and identify novel drug targets and diagnostic markers.

2016-01-12 | E-MTAB-4029 | biostudies-arrayexpress

Kinase activities in pancreatic ductal adenocarcinoma with prognostic and therapeutic avenues

Project description:The aim of this experiment is to unravel PDAC biology and phospho-print based on aberrant kinase activities and proteome alterations. For this we will perform pTYyrIP, Bravo_IMAC, and protein expression data of n=56 tissues encompassing 47 pancreatic ductal adenocarcinoma (PDAC), 5 cholangiocarcinoma, 1 Intraductal Papillary Mucinous Neoplasm (IPMN), 1 pancreatitis and 1 pancreatitis-Pancreatic Intraepithelial Neoplasia (PanIN) tissue. Pancreatitis, PanIN, and IPMN are seen as early events predecessing PDAC. An equiproportional pool of 5 PDAC cell lines (PANC1, SUIT-2, CFPAC-1, HPAC, MIAPACA2) is also taken along.

2024-04-23 | PXD043111 | Pride

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