Transcriptional profile analysis of Caco-2 cell line upon inflammatory signals and ER stress induction
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ABSTRACT:
PROVIDER: PRJNA825555 | ENA |
REPOSITORIES: ENA
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Project description:We stimulated Caco-2 cells, with the TLR5 agonist flagellin (Fl), with the chemical ER stress inducer thapsigargin (TG), or a combination of both (TGFl). This strategy mimics a pro-inflammatory response in the presence of ER stress.
2022-04-16 | GSE200626 | GEO
Project description:To investigate the role of p53 and DICER in the induction of ER stress, wildtype, p53 knockout or DICER mutant HCT116 colon cancer cells were treated with the ER stress inducers tunicamycin or brefeldin A for 24 hours. Microarray analysis was used to determine changes in gene expression associated with the induction of ER stress, and to compare this induction in wildtype, p53 knockout or DICER mutant HCT116 colon cancer cells
2015-04-01 | GSE63252 | GEO
Project description:To investigate the role of p53 and DICER in the induction of ER stress, wildtype, p53 knockout or DICER mutant HCT116 colon cancer cells were treated with the ER stress inducers tunicamycin or brefeldin A for 24 hours. Microarray analysis was used to determine changes in gene expression associated with the induction of ER stress, and to compare this induction in wildtype, p53 knockout or DICER mutant HCT116 colon cancer cells Triplicate samples of HCT116 wildtype, HCT116 p53 knockout and HCT116 DICEREX5/EX5 cells were treated with with 0.5 mg/ml of BFA or 2 mg/ml of Tm for 24 h. Following treatment, cells were harvested and lysed in TRIzol reagent and RNA was extracted. Microarray analysis was carried out using Affymetrix HG-U133_Plus-2 arrays.
2015-04-01 | E-GEOD-63252 | biostudies-arrayexpress
Project description:Objective: We previously showed that Campylobacter jejuni Cas9 was necessary for full virulence and efficient induction of human cell stress followed by cell death, but no virulence mechanism could be unravelled then. Therefore, we carried out global genome-wide transcriptomics, using RNA samples extracted from cells infected by a wild-type C. jejuni strain and the corresponding cas9 deletion strain. Methods: Caco-2 epithelial cells were infected with C. jejuni wild-type or cas9 deletion strains and RNA was extracted at 5 timepoints post-infection. Results: Wild-type C. jejuni induced cellular stress, DNA damage and cell death pathways in Caco-2 cells continuously from 30 min up to 4 hours after infection, eventually followed by visual cell death induction after 24 hours; the corresponding cas9 deletion strain did also induce cell stress pathways within the first two hours of infection but at later timepoints, stress pathway induction had dropped and after 4 hours of infection, expression of the corresponding stress genes had normalised to near-t=0 (uninfected) expression values; the cas9 deletion strain did not lead to visual cell death induction after 24 hours. Conclusions: Campylobacter jejuni Cas9 is necessary for full virulence of C. jejuni and is involved in the efficient induction of cellular stress pathways and eventually, cell death.
2018-09-30 | GSE89661 | GEO
Project description:Dynamic changes in the endoplasmic reticulum (ER) morphology are central to maintaining cellular homeostasis. Microtubules (MT) facilitate the continuous remodeling of the ER network into sheets and tubules by coordinating with many ER-shaping protein complexes, although how this process is controlled by extracellular signals remains unknown. Here we report that TAK1, a kinase responsive to various growth factors and cytokines including TGF- and TNF-, triggers ER tubulation by activating TAT1, an MT-acetylating enzyme that enhances ER-sliding. We show that this TAK1/TAT1-dependent ER remodeling promotes cell survival by actively downregulating BOK, an ER membrane-associated proapoptotic effector. While BOK is normally protected from degradation when complexed with IP3R, it is rapidly degraded upon their dissociation during the ER sheets-to-tubules conversion. These findings demonstrate a distinct mechanism of ligand-induced ER remodeling and suggest that the TAK1/TAT1 pathway may be a key target in ER stress and dysfunction.
2024-06-16 | PXD045865 | Pride
Project description:The ruthenium-based anticancer agent BOLD-100/KP1339 has shown promising results in several in vitro and in vivo tumour models, as well as in early clinical trials. However, its mode of action remains to be fully elucidated. Recent evidence identified ER stress-induction and concomitant down-modulation of HSPA5 (GRP78) as key drug effects. By exploiting the naturally formed adduct between BOLD-100 and human serum albumin as an immobilization strategy, we were able to perform target profiling experiments that revealed the ribosomal proteins RPL10, RPL24 and the transcription factor GTF2I as potential interactors of this ruthenium(III) anticancer agent. Integrating these findings with proteomic profiling and transcriptomic experiments supported ribosomal disturbance and concomitant induction of endoplasmic reticulum (ER) stress. The formation of poly-ribosomes and ER swelling of treated cancer cells by electron microscopy validated this finding. Thus, the direct interaction of BOLD-100 with ribosomal proteins seems to accompany ER stress-induction and modulation of GRP78 in cancer cells.
2021-06-01 | PXD022449 | Pride
Project description:WNT signals inhibit paracrine induction of senescence in human multipotent stromal cells
| PRJNA638361 | ENA
Project description:Previously, we constructed a coculture model to analyze the effect of macrophages on intestinal epithelial cells, and found that TNF-a secreted from human macrophage-like THP-1 cells induced cell damage to intestinal epithelial Caco-2 cells (Exp.Cell.Res. 2006, 312(19):3909-19). In this study, we present activation of NF-kB in Caco-2 cells within 15 min after coculturing. To reveal how TNF-a secreted from THP-1 cells affects Caco-2 cells in an early stage of coculture, we exhaustively analyzed the changes of gene expression in Caco-2 cells cocultured with THP-1 cells over the time periods of 0, 1, 3, 6, 24, and 48 h by using a DNA microarray. Differentially expressed genes extracted with maSigPro demonstrated that IEX-1 was the lowest p-value gene, that is, the most significantly changed gene among the up-regulated genes. The genes expressed in a similar pattern to IEX-1 involved immunity, apoptosis, and protein kinase cascade. These findings suggest that the stimuli of TNF-a from THP-1 cells activates NF-kB, leading induction of various gene expression. This pattern of gene expression indicates that not only early defense response but also cell death occurs at the same time, causing inflammatory condition.
2010-03-08 | GSE17625 | GEO
Project description:Previously, we constructed a coculture model to analyze the effect of macrophages on intestinal epithelial cells, and found that TNF-a secreted from human macrophage-like THP-1 cells induced cell damage to intestinal epithelial Caco-2 cells (Exp.Cell.Res. 2006, 312(19):3909-19). In this study, we present activation of NF-kB in Caco-2 cells within 15 min after coculturing. To reveal how TNF-a secreted from THP-1 cells affects Caco-2 cells in an early stage of coculture, we exhaustively analyzed the changes of gene expression in Caco-2 cells cocultured with THP-1 cells over the time periods of 0, 1, 3, 6, 24, and 48 h by using a DNA microarray. Differentially expressed genes extracted with maSigPro demonstrated that IEX-1 was the lowest p-value gene, that is, the most significantly changed gene among the up-regulated genes. The genes expressed in a similar pattern to IEX-1 involved immunity, apoptosis, and protein kinase cascade. These findings suggest that the stimuli of TNF-a from THP-1 cells activates NF-kB, leading induction of various gene expression. This pattern of gene expression indicates that not only early defense response but also cell death occurs at the same time, causing inflammatory condition. Caco-2 cells were cultured for 14 days on a semi-permeable support, and THP-1 cells were differentiated with phorbol myristate acetate (PMA) for 4 days in 12-well plates. Then, the semi-permeable support membrane in which Caco-2 cells had been cultured was placed on the 12-well plates on which THP-1 has been cultured.
2010-04-06 | E-GEOD-17625 | biostudies-arrayexpress
Project description:Upon infection of a mammalian host, Plasmodium parasites first replicate inside hepato-cytes, generating thousands of new parasites. Although Plasmodium intra-hepatic devel-opment represents a substantial metabolic challenge to the host hepatocyte, how infected cells respond to and integrate this stress remains poorly understood. Here, we present proteomic and transcriptomic analysis revealing that the endoplasmic reticulum (ER)-resident unfolded protein response (UPR) is activated in host hepatocytes upon Plasmo-dium berghei infection. The expression of XBP1s -the active form of the UPR mediator XBP1- and the liver-specific UPR mediator CREBH is induced by P. berghei infection in vivo. Furthermore, this UPR induction increases parasite liver burden. Altogether, our data suggests that ER stress is a central feature of P. berghei intra-hepatic development, contributing to the success of infection.
2016-04-20 | PXD002269 | Pride