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Gene expression analysis in Panc-1 cells in response to treatment with Gli3T, a dominant-negative repressor of Gli

ABSTRACT: Pancreatic Ductal Adenocarcinoma (PDAC) is one of the most aggressive human malignancies. In our studies, we find that the Gli transcription factors are required for Kras initiation of pancreatic tumorigenesis. In order to identify the downstream transcriptional targets of Gli in PDAC, we conducted gene expression analysis using Gli3T, a transcriptional repressor of Gli. In this data set we include the expression data from 6 samples with three of them expressing a control vector and another three expressing Gli3T

ORGANISM(S): Homo sapiens

PROVIDER: GSE36855 | GEO | 2012/03/29

SECONDARY ACCESSION(S): PRJNA157135

REPOSITORIES: GEO

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Gene expression analysis in Panc-1 cells in response to treatment with Gli3T, a dominant-negative repressor of Gli

Project description:Pancreatic Ductal Adenocarcinoma (PDAC) is one of the most aggressive human malignancies. In our studies, we find that the Gli transcription factors are required for Kras initiation of pancreatic tumorigenesis. In order to identify the downstream transcriptional targets of Gli in PDAC, we conducted gene expression analysis using Gli3T, a transcriptional repressor of Gli. In this data set we include the expression data from 6 samples with three of them expressing a control vector and another three expressing Gli3T Gli3T with IRES-GFP, or an empty vector was ectopically expressed in Panc-1 cells using lipofectamine transfection. GFP positive cells were sorted 24 hours post transfection and RNA was isolated from the cells using Qiagen RNAeasy kit. Affymetrix gene expression array was conducted on the Panc-1 cells expressing the control vector and cells expressing Gli3T. Relative gene expression between the two sample sets was analyzed. Three samples were analyzed for each set.

2012-03-28 | E-GEOD-36855 | biostudies-arrayexpress

Regulation of GLI underlies a role for BET bromodomains in pancreatic cancer growth and the tumor microenvironment

Project description:Pancreatic ductal adenocarcinoma (PDAC) is extraordinarily chemoresistant and the abundant stromal content of these tumors contributes to the ineffective treatment of this disease. While the genetic alterations of PDAC have been well characterized, the epigenetic pathways regulating PDAC remain, for the most part, elusive. Employing an in vivo shRNA screen targeting epigenetic regulators, we identified members of the BET family of chromatin adaptors as key regulators of PDAC cell growth and maintenance of the tumor stroma. BET family members contribute to PDAC cell growth by modulating the activity of two key transcriptional programs, MYC and GLI. Within the cancer cells, BET inhibition also results in down-regulation of a key mediator of the tumor microenvironment, SHH, corresponding to a decrease in the stromal content of tumors. Taken together, these results suggest that therapeutic inhibition of BET proteins offers a novel mechanism to target both the neoplastic and stromal components of PDAC. Total RNA was isolated from 4 untreated PDAC cell lines or those exposedto the BET bromodomain inhibibitor CPI203 (1.6 uM) or control DMSO for 5 and 10 hours

2016-09-08 | E-GEOD-55209 | biostudies-arrayexpress

Regulation of GLI underlies a role for BET bromodomains in pancreatic cancer growth and the tumor microenvironment

2016-09-08 | GSE55209 | GEO

Gene expression analysis between the pancreatic tissues of Pdx1-cre;Kras LSL-G12D and Pdx-cre;KrasLSL-G12D;IKK2/beta F/F mice

Project description:Constitutive Kras and NF-kB activation is identified as signature alterations in human pancreatic ductal adenocarcinoma (PDAC). Here, we report that pancreas-targeted IKK2/beta inactivation inhibited NF-kB activation and completely suppressed PDAC development. Our findings demonstrated that NF-kB is required for development of pancreatic ductal adenocarcinoma that was initiated by Kras activation. Pancreatic tissue from 4 groups of mice were used in this project: (1) the pancreas normal appearance of Pdx1-cre;KrasLSL-G12D;IKK2/beta mice, (2) the normal pancreas of Pdx1-cre;KrasLSL-G12D mice, (3) the pancreatic lesion of pancreatic intraepithelial neoplasia (PanIN) of Pdx1-cre;KrasLSL-G12D mice, and (4) the pancreatic lesion of PDAC of Pdx1-cre;KrasLSL-G12D mice. Each group included three mice. RNA samples from mouse pancreas were hybridized on GeneChip Mouse Gene 1.0 ST arrays (Affymetrix). Group (1) and group (2) were compared, and group (2), group (3) and group (4) were compared.

2012-01-24 | E-GEOD-33322 | biostudies-arrayexpress

Combinatorial Gli activity directs immune infiltration and tumor growth in pancreatic cancer

Project description:Proper Hedgehog (HH) signaling is essential for normal embryonic and postnatal development, while de-regulated HH signaling drives numerous pediatric and adult cancers. In pancreatic cancer, paracrine HH signaling from tumor cells to fibroblasts contributes to tumor progression. However, the role of HH signaling in pancreatic cancer remains controversial, with both tumor-promoting and tumor-restraining functions reported. Notably, the GLI family of transcription factors (GLI1, GLI2, GLI3), key downstream effectors of HH signaling, remain poorly understood in pancreatic cancer. In this study we investigated the individual and combined roles of GLI1-3 in pancreatic cancer progression. Inducible, fibroblast-specific deletion of Gli2 and Gli3 in a mouse model of pancreatic cancer progression reduces collagen deposition and decreases immunosuppressive myeloid cell infiltration. Further, Gli2 and Gli3 deletion leads to an increase in T cells during PanIN stages and an increase in NK cells in implanted tumors, which in turn suppresses tumor growth. Surprisingly, combined loss of all three Glis leads to a widespread loss of acinar cells, an increase in macrophage infiltration, and an increase in tumor growth. Together, these data indicate that a baseline level of Gli is necessary to maintain proper balance of cell types in the pancreas, and the coordinated activity of GLI1-3 directs the fibroinflammatory response in pancreatic cancer.

2022-07-05 | GSE185748 | GEO

The miRNA profiling in PANC-1, PANC-1 GEM 100 and PANC-1 GEM1500 cells

Project description:Gemcitabine has been a first-line therapeutic agent for pancreatic ductal adenocarcinoma (PDAC) pancreatic cancer; however, acquisition of resistance to gemcitabine remains a major challenge. We analyzed miRNAs expression profiles by array-based miRNAs analysis between gemcitabine–resistant (PANC-1/GEM) and parental PANC-1 cells.

2016-12-31 | GSE79234 | GEO

Pten deficiency cooperates with KrasG12D to activate NFkB pathway promoting the development of malignant pancreatic ductal adenocarcinoma

Project description:Almost all human pancreatic ductal adenocarcinomas (PDACs) are driven by oncogenic Kras and the progression of the disease is characterized by the serial appearance of certain genetic lesions. Mouse models have convincingly shown that Kras mutation induces classical PanIN lesions that can progress to PDAC in the appropriate tumor suppressor background. However, the cooperative mechanism between mutant Kras-dependent signaling surrogates and other oncogenic pathways remains to be fully elucidated in order to devise better therapeutic strategy. Mounting evidence PTEN/PI3K perturbation on PDAC tumorigenesis, we observed frequent PTEN inactivation at both genomic and histopathological levels in primary human PDAC samples. The importance of PTEN/PI3K pathway during the development of PDAC was further supported by genetic studies demonstrating that Pten deficiency in cooperation with Kras activation accelerated the formation of invasive PDAC. Mechanistically, combined Kras mutation and Pten inactivation leads to NFkB activation and subsequent induction of cytokine pathways, accompanied with strong stromal activation and immune cell infiltration. Therefore, PTEN/PI3K pathway dictates the activity of NFkB network and serves as a major surrogate during Kras-mediated pancreatic tumorigenesis. Primary pancreatic ductal epithelial cell cultures were established from 6 week old Pdx1-Cre;LSL-KrasG12D L/+ (n=3) or Pdx1-Cre;LSL-KrasG12D L/+;Pten L/+ (n=5) mice. Total RNA was collected from early passage cells.

2011-08-31 | E-GEOD-25828 | biostudies-arrayexpress

Analysis of the impact of Nucleolin phospho-mutants on the proteome of pancreatic ductal adenocarcinoma cells.

Project description:To reveal the impact of Nucleolin (Ncl) phosphorylation on oncogenic KRAS-induced changes in the proteome of Pancreatic Ductal Adenocarcinoma (PDAC) cells, we carried out a quantitative proteomic analysis on tumour cells isolated from an inducible mouse model of PDAC (iKras PDAC) (Ying et al., 2012), which were ectopically expressing wild-type or different phospho-mutants of Ncl. In this mouse model, oncogenic Kras (G12D) expression can be controlled by administration of doxycycline (Dox). Tandem Mass Tagging (TMT) was employed for quantitative analysis of Dox induced (24hrs) vs. non-induced iKras-PDAC cells, which were privously transfected with three different expression constructs of mouse myc-tagged Ncl. These constructs encoded for wild-type Ncl (WT Ncl), a phospho-defective mutant with four Serine to Alanine mutations on S28, S34, S41, and S42 sites (S4A Ncl), and a phospho-mimicking mutant with the same Serines mutated to Aspartic Acid (S4D Ncl). Cells were subjected to whole cell lysis, followed by Trypsin digestion, TMT barcoding with TMT 6plex kit (Thermo), and peptide fractionation, before analysis by LC-MS/MS.

2023-02-12 | PXD038496 | Pride

Proteogenomic Network Analysis of Context-Specific KRAS Signaling In Mouse-to-Human Cross-Species Translation

Project description:The highest frequencies of KRAS mutations occur in colorectal carcinoma (CRC) and pancreatic ductal adenocarcinoma (PDAC). Therapeutically targeting downstream pathways mediating oncogenic properties of KRAS mutant cancers is limited by an incomplete understanding of the contextual cues modulating the signaling output of activated KRAS. We performed mass spectrometry on mouse tissues expressing wild-type or mutant KRAS to determine how tissue context and genetic background modulate oncogenic signaling. Mutant KRAS dramatically altered the proteomes and phosphoproteomes of pre-neoplastic and neoplastic colons and pancreases in a largely context-specific manner. We developed an approach to humanize the mouse networks with data from human cancer and identified genes within the CRC and PDAC networks synthetically lethal with mutant KRAS. Our studies demonstrate the context-dependent plasticity of oncogenic signaling, identify non-canonical mediators of KRAS oncogenicity within the KRAS-regulated signaling network, and demonstrate how statistical integration of mouse and human datasets can reveal cross-species therapeutic insights.

2019-06-28 | PXD013922 | Pride

Identification of GLI-associated proteins by mass spectrometry

Project description:The Hedgehog signaling pathway is essential for the maintenance and response of several types of stem cells. To study the transcriptional response of stem cells to HH signaling, we searched for proteins binding to GLI proteins, the transcriptional effectors of the HH pathway in mouse embryonic stem (ES) cells. We purified GLI protein complex from an ES cell line that contained a tamoxifen-inducible 3XFLAG-tagged GLI3 repressor allele by anti-FLAG immunoprecipitation and several novel GLI co-factors were identified in the complex by subsequent mass spectrometry analysis.

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