Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of human pancreatic duct epithelial cell line (H6c7) Gene expression changes induced by K-ras oncogene in the

ABSTRACT: k-ras oncogene was transduced into the HPV16-E6E7 immortalized normal human pancreatic duct epithelial cell line (H6c7) to generate a stable K-ras oncogene-expressing cell line (H6c7-Kr). The gene expression profile of the H6c7-Kr cells was compared to that of H6c7 cells. We have excluded (subtracted) genes that were deregulated by transduction of the construct used for K-ras oncogene expression.

ORGANISM(S): Homo sapiens

SUBMITTER: Ming-Sound Tsao

PROVIDER: E-GEOD-1955 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

In vitro modeling of human pancreatic duct epithelial cell transformation defines gene expression changes induced by K-ras oncogenic activation in pancreatic carcinogenesis.

Qian Jiaying J Niu Jiangong J Li Ming M Chiao Paul J PJ Tsao Ming-Sound MS

Cancer research 20050601 12

Genetic analysis of pancreatic ductal adenocarcinomas and their putative precursor lesions, pancreatic intraepithelial neoplasias (PanIN), has shown a multistep molecular paradigm for duct cell carcinogenesis. Mutational activation or inactivation of the K-ras, p16(INK4A), Smad4, and p53 genes occur at progressive and high frequencies in these lesions. Oncogenic activation of the K-ras gene occurs in >90% of pancreatic ductal carcinoma and is found early in the PanIN-carcinoma sequence, but its ...[more]

PMID: 15958547

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Project description:This experiment was designed to study oncogene-induced senescence (OIS). To this end we generated a series of cell lines derived from normal human diploid fibroblasts IMR90 forced to express the catalytic subunit of telomerase (hTERT). This cells were then subjected to further manipulation by orderly introducing defined genetic elements by retroviral transduction. The first cell line generated was ITV, which was obtained from the original cell line (IMR90 with hTERT) after introducing an empty vector. Subsequently, we introduced Mek:ER, which is a switchable version of the Mek kinase, a relevant downstream effector of Ras signaling during Ras-induced senescence, to generate ITM cells. We further modified this cell line by introducing SV40 small-t antigen (ST), papillomavirus oncoproteins E6 and E7 (E6/E7) or the combination of both (E6/E7 and ST). In this manner, we obtained ITMST, ITME6E7 and ITME6E7ST respectively. This cellular system allow us to have a representation of the different steps into neoplastic transformation. ITM and ITMST cells respond to Mek activation by inducing OIS. ITME6E7 and ITME6E7ST cells do not enter OIS after Mek activation. Mek activation is achieved by treating all cell cultures with 4-hydroxytamoxifen (4OHT) at 100 nM, in the absence of serum, and for 3 days. The gene expression profile of ITV cells served as a reference for all the expression values obtained with the rest of the cell lines. Thus, we ended up with the expression profiles of two cell lines representing oncogene-induced senescence (ITM and ITMST), and two cell lines representing bypass of oncogene-induced senescence, plus a reference profile provided by ITV, the cell line from which all the other cell lines were derived. Our final goal was to identify markers of the oncogene-induced senescence response by comparing the expression profiles of the cell lines entering OIS after Mek activation (that is, after 4OHT treatment) with the ones bypassing this response. Keywords: other

Dataset Information

Transcription profiling of human pancreatic duct epithelial cell line (H6c7) Gene expression changes induced by K-ras oncogene in the

Publications

In vitro modeling of human pancreatic duct epithelial cell transformation defines gene expression changes induced by K-ras oncogenic activation in pancreatic carcinogenesis.

Similar Datasets

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