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Gene expression profile upon TNF-a stimulation, forced expression of NICD, or TNF-a stimulation under forced expression of NICD, in human colon carcinoma-derived LS174T cells

ABSTRACT: Gene expression profile upon TNF-a stimulation, forced expression of NICD, or TNF-a stimulation under forced expression of NICD, in human colon carcinoma-derived LS174T cells

PROVIDER: PRJNA484183 | ENA |

REPOSITORIES: ENA

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Gene expression profile upon TNF-a stimulation, forced expression of NICD, or TNF-a stimulation under forced expression of NICD, in human colon carcinoma-derived LS174T cells

Project description:A human colon carcinoma-derived cell line LS174T was modified to overexpress NICD, intracellular domain of Notch1, upon doxycycline addition (designated as LS174T-tetON-NICD cells), using the T-rex system (Invitrogen). We have previously shown that these cells can overexpress NICD under the control of CMV promoter (Okamoto R et al, Am J Physiol, 296(1):G23-35, 2009), and the amont of the overexpressed NICD protein reaches to the maximal level in early as 3 hours from doxycycline addition (100ng/ml), which persists for up to 24 hours. In the present experiment, LS174T-tetON-NICD cells were treated with recombinant human TNF-a (50ng/ml) alone, doxycycline alone (100ng/ml), co-treated by both TNF-a and doxycycline, or left untreated (Control) for 24 hours, and subjected for analysis. Experiment was done using a modified sub-line of LS174T cell (LS174T-tetON-NICD cells), in which overexpression of NICD can be induced by a Doxycycline dependent manner.

2018-12-31 | GSE118048 | GEO

Gene expression profile upon IL-22 stimulation, forced expression of Hes1, or IL-22 stimulation under forced expression of Hes1, in human colon carcinoma-derived LS174T cells

Project description:A human colon carcinoma-derived cell line LS174T was modified to overexpress Hes1, a bHLH-type transcription factor, upon doxycycline addition (designated as LS174T-tetON-Hes1 cells), using the T-rex system (Invitrogen). We have previously shown that these cells can overexpress Hes1 under the control of CMV promoter (Zheng et al, Inflamm Bowel Dis, 17;2251-2260, 2011), and the amont of the overexpressed Hes1 protein reaches to the maximal level in early as 3 hours from doxycycline addition (100ng/ml), which persists for up to 24 hours. In the present experiment, LS174T-tetON-Hes1 cells were treated with recombinant human IL-22 (20ng/ml) alone, doxycycline alone (100ng/ml), co-treated by both IL-22 and doxycycline, or left untreated (Control) for 24 hours, and subjected for analysis. Experiment was done using a modified sub-line of LS174T cell (LS174T-tetON-Hes1 cells), in which overexpression of Hes1 can be induced by a Doxycycline dependent manner. Four-condition experiment, Control vs. IL-22 stimulation, Control vs Doxycycline addition (Hes1 overexpression) and Control vs IL22 stimulation+Doxycycline addition (Hes1 overexpression). Biological replicates: One for each condition, independently grown and harvested. One replicate per array.

2013-10-01 | E-GEOD-43012 | biostudies-arrayexpress

Gene expression profile upon IL-22 stimulation, forced expression of Hes1, or IL-22 stimulation under forced expression of Hes1, in human colon carcinoma-derived LS174T cells

2013-10-01 | GSE43012 | GEO

TGFβ reprograms TNF stimulation of macrophages towards osteoclastogenesis

Project description:TGFβ reprograms TNF stimulation of macrophages towards osteoclastogenesis

| PRJNA721177 | ENA

Expression analysis of KHR and KHR-NICD oral tumors

Project description:KHR-NICD oral tumors grow faster than KHR oral tumors. The hypothesis was to test for differences in gene expression between KHR and KHR-NICD oral tumors.

2015-09-09 | GSE59950 | GEO

Expression analysis of KHR and KHR-NICD oral tumors

Project description:KHR-NICD oral tumors grow faster than KHR oral tumors. The hypothesis was to test for differences in gene expression between KHR and KHR-NICD oral tumors. Total RNA was isolated for KHR (n=6) and KHR-NICD (n=6) oral tumors. Expression profiling was performed using the Illumina MouseRef-8 v2 (GPL6885) array. Studies were conducted using tumors from FVB x C57BL/6 F1 mice.

2015-09-09 | E-GEOD-59950 | biostudies-arrayexpress

mRNA-seq of HCT116 RNF40 knockdown cells upon TNF-alpha stimulation

Project description:This analysis identifies genes which are affected upon RNF40 knockdown cells and/or TNF-alpha stimulation

2018-10-22 | E-MTAB-7197 | biostudies-arrayexpress

Gene expression changes in Nicd induced wing disc hyperplasia

Project description:The outcome of Notch proliferation on proliferation depends on the context. In Drosophila wing imaginal discs Notch activation causes hyperplasia despite having localized inhibitory effects on proliferation. To understand te underlying mechanisms we have used genomic strategies to identify the Notch-Su(H) target genes during wing discs hyperplasis. these data are the results from expression profiling the RNAs from hyperplastic wing discs overexpressing Nicd. Direct comparison of third instar lavae wing imaginal disc Nicd (abxUbxFLPase; Act>y>Gal4, UAS GFP; FRT82B tubGal80 with UAS-Nicd; FRT82B) vs control (abxUbxFLPase; Act>y>Gal4, UAS GFP; FRT82B tubGal80 with FRT82B ). 4 Biological replicates, the 2nd replicate was performed as a dye-swap.

2013-12-31 | E-GEOD-41428 | biostudies-arrayexpress

Transcriptome profiling of Drosophila wild type and ttk-RNAi, dpn overexpressed, Nicd overexpressed and seq&Nicd overexpressed intestinal progenitor cells

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare transcriptome profiling (RNA-seq) of intestinal progenitor cells in Drosophila wild type and ttk-RNAi, dpn overexpressed, Nicd overexpressed and seq&Nicd overexpressed midguts Methods: mRNA profiles of intestinal progenitor cells isolated from 7-day-old wild-type (Ctrl) and ttk-RNAi, dpn overexpressed(dpn OE), Nicd overexpressed(Nicd OE) and seq&Nicd overexpressed(seq&Nicd OE) Drosophila midgut were generated by deep sequencing using Illumina HiSeq 2500. Results: ttk-RNAi in intestinal progenitor cells induces the expression of many neural-specific genes, including dpn and seq. Dpn ectopic expresion explains most of the ttk-RNAi expression profile change. Seq ectopic expression explains the expression of neural-specific Notch targets in the ttk-RNAi intestinal progenitor cells.

2021-02-23 | GSE130942 | GEO

Gene expression analysis of SJG6 CONTROL and NICD

Project description:Mutational landscape of Oral Squamous Cell Carcinoma (OSCC) is predominated by frequent inactivating mutations in EGF- like ligand binding domain of NOTCH1. However role of NOTCH1 signalling in tumorigenesis is highly context and cell type dependent. In this study, we investigated phenotypic effect of NOTCH1 mutations in primary line derived from OSCC biopsy. Based on gain-of-function assays in NOTCH1 mutant line we demonstrated regulation of cell behaviour and morphology, by NOTCH1 intracellular domain (NICD) leading to changes in cell proliferation, migration, clonal growth and differentiation. Importantly, overexpression of NICD results in upregulation of ETV7/TEL2 which negatively regulates SERPINE1 expression and confers malignant cells with less aggressive phenotype. Further knockdown of SERPINE1 expression simulated the phenotypes observed upon rescue of NICD. In accord with our cell-based model we observed strong correlation between NOTCH1, ETV7 and SERPINE1 expression in OSCC primary tumours indicating similar deregulated mechanisms during oral carcinogenesis. Overall this study suggests a tumour suppressive role of NOTCH1 in OSCC and highlights possible mechanisms leading to changes in cell behaviour and morphology in absence of NICD potentially by regulating TEL2 and SERPINE1 expression.

2019-03-05 | GSE127770 | GEO

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