Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA273444 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1770400.fastq.gz | Fastqsanger.gz | |||
| SRR1770401.fastq.gz | Fastqsanger.gz | |||
| SRR1770402.fastq.gz | Fastqsanger.gz | |||
| SRR1770403.fastq.gz | Fastqsanger.gz | |||
| SRR1770404.fastq.gz | Fastqsanger.gz |
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2018-01-22 | GSE65193 | GEO
Project description:The activation of the NF-κB-JNK pathway is independent of the PI3K-Rac1-JNK pathway involved in the bFGF-regulated human fibroblast cell migration
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Project description:Cancer cell invasion and subsequent metastasis accounts for most cancer related deaths. However, despite recent progress, there is a need to understand how the main pathways involved in oncogenic cell invasion and metastasis amalgamate into multifunctional networks. Using functional transcriptomic analysis of Drosophila Ras oncogenic hindgut enterocytes, we identified a feed-forward loop between the Toll/NF-κB innate immune pathway and Rac1 signaling driving actin cytoskeleton rearrangements, basement membrane degradation, and loss of intercellular adhesion. We find that this network is necessary and sufficient to promote oncogenic hindgut enterocyte invasion and dissemination. The network is orchestrated by Rac1, which promotes actin cytoskeleton alterations, JNK-mediated matrix metalloprotease-mediated basement membrane degradation and Toll-Snail-depended E-cadherin repression, leading to epithelial-to- mesenchymal transition and dissemination. However, Toll pathway positively regulates itself and the Rac1 pathway cytoskeletal genes downstream of the Ras oncogene, while JNK signaling alone does not suffice to induce cell dissemination. The tight crosstalk between Toll and Rac1 pathways reveals an integral role of Toll/NF-κB in Ras-initiated oncogenic epithelial cell migration.
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Project description:Cordyceps participates in various pharmacological activities including anti-tumor, and is involved in the regulation of NF-κB signaling pathway. However, the detailed role of cordycepin in suppression of NF-κB signaling pathway is less clear. In this study, we first analyzed the effect of cordyceps on NF-κB activity in TK-10 cells, and found that cordyceps resulted in a dose-dependent reduction in TNF-α-induced NF-κB activation. Here, we show that cordyceps mediated NF-kB inhibition induces apoptosis in TK-10 cells involved the serial activation of caspases. Moreover, we demonstrate that in addition to activating caspases, the cordyceps negatively modulates TNF-α-mediated NF-κB signaling to promote JNK activation, which results in apoptosis, and that NF-kB regulates antiapoptotic factor GADD45b and the JNK kinase MKK7. When the TNFα cytokine binds to the TNF receptor, IκB dissociates from NF-κB. As a result, the active NF-κB translocates to the nucleus. Cordyceps clearly prevented NF-κB from mobilizing to the nucleus, resulting in downregulation of GADD45b, whereas upregulation of MKK7 and phosphorylation of JNK (p-JNK). This increased Bax activation, leading to marked cordyceps-induced apoptosis. Bax subfamily proteins induced apoptosis through caspase-3. Furthermore, siRNA mediated inhibition of MKK7 downregulated p-JNK and The JNK inhibitor SP600125 strongly inhibited Bax. Thus, these results indicate that cordyceps inhibits NF-κB/GADD45b signaling activation to upregulate MKK7-JNK signaling pathway to induce apoptosis in TK-10 cells and support the potential of cordyceps as a therapeutic agent for renal cancer.
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Project description:The activated B-cell–like (ABC) subtype of diffuse large B-cell lymphoma (DLBCL) represents a very aggressive human lymphoma entity. Constitutive NF-κB activation caused by chronic active B-cell receptor (BCR) signaling is common feature of many ABC DLBCL cells; however, the pathways linking BCR signaling to the NF-κB prosurvival network are largely unknown. Here we report that constitutive activity of PI3K and the downstream kinase PDK1 are essential for the viability of two ABC DLBCL cell lines that carry mutations in the BCR proximal signaling adaptor CD79B. In these cells, PI3K inhibition reduces NF-κB activity and decreases the expression of NF-κB target genes. Furthermore, PI3K and PDK1 are required for maintaining MALT1 protease activity, which promotes survival of the affected ABC DLBCL cells. These results demonstrate a critical function of PI3K-PDK1 signaling upstream of MALT1 pro- tease and NF-κB in distinct ABC DLBCL cells and provide a rationale for the pharmacologic use of PI3K inhibitors in DLBCL therapy.
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Project description:Transplantation of functional neurons improve the functionally recovery in animal models of Alzheimer's disease and other neurological disorders. Although functional neurons can be differentiated from embryonic stem cells or induced-pluripotent stem cells, alternative cell sources of functional neurons may be more available for transplantation. Dedifferentiated fat cells (DFATs) were isolated and cultured from mature adipose tissue, which have advantages in their abundance, ease of isolation and homogeneity compared to other adult stem cells. DFATs are promising for clinical applications such as cell transplation therapy. Direct reprogramming has been developed in recent years. It is possible to convert mature differentiated cells into other types of functional cells by introducing cell-fate-conversion transcriptional factors. However, the introduction of exogenous transcriptional factors limits their use of clinical application. Previous studies found that in vitro neuronal differentiation follows the processes of in vivo neuronal development, which are related to the surrounding microenvironments. Therefore, the arrangement of a proper microenvironment for the neuronal development process is essential to induce neuronal differentiation. In this study, we report that DFATs differentiated into neurons by all trans retinoic acid (ATRA) and basic fibroblast growth factor (bFGF). The ATRA/bFGF-treated DFATs expressed the neuron-specific mRNA and pritein expression, exibited neuron-like morphology, generated voltage-dependent sodium current and action potentials and react with neurotransmitters. Transcriptomics resutls suggested that ATRA/bFGF treatment induced a specific differentiatioin into neurons. The lesional analysis revealed that ATRA/bFGF-treated cells are compatible with telemcephalon gabaergic neuron. To investigate the mechanism of ATRA/bFGF-induced neuronal differentiation, we performed the pathway analysis. The pathway analysis suggested that JNK signaling pathway was involved in the neuronal diffeerentiation. Our knockdown experiient further demonstrated that JNK3, a neuronal subtype of JNK, plays a crucial role in ATRA/bFGF-induced neuronal differentiation. In conclusion, we demonstrated that ATRA/bFGF induced DFATs into functional neurons via the activation of JNK3 signaling pathway. Our study provides an efficient approach for generating functional neurons from adult fat tissue and reveals the functional importance of JNK3 in neuronal differentiation process.
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Project description:Although therapy responsiveness to therapy in Burkitt lymphoma (BL) is high, relapsed disease and and chemoresistance remain a clinical challenge, and complete mechanisms underlying BL chemoresistance and how it can be circumvented is yet to be fully elucidated. In this study we present data showing that chymotrypsin-like serine proteases inhibitor Nα-tosyl-L-phenylalanine chloromethylketone (TPCK) and specific NF-κB inhibitor Bay-11 7082 can induce caspase-independent apoptosis in chemoresistant BL cells. We also demonstrate that both TPCK and Bay-11 7082-treatment leads to decreased NF-κB nuclear activity and that this is associated with sensitization of chemoresistant Burkitt lymphoma cells. Furthermore we investigated global transcriptional changes induced by Bay-11 7082 and TPCK in the DG-75 and Raji cell lines, respectively, by microarray analysis using Illumina BeadChips. TPCK-treatment of Raji and DG-75 cells resulted in 59 and 21 differently expressed genes, respectively, while Bay-11-treated Raji and DG-75 cells displayed 1403 and 8 differently expressed genes, respectively. Gene Ontology (GO) categorization confirmed enrichment of multiple GOs in Bay 11-treated Raji and DG-75 cells. Fifty percent of the 61 categories in Raji cells were categories sorting under Biological Processes and represented mostly increased gene expression. In DG-75 cells Bay-11 7082 induced significant gene ontology enrichment in only two categories, where the increased/decreased ratio was 1:1. Further unsupervised and supervised bioinformatics processing by Ingenuity Pathway Analysis indicated significant networks in response to TPCK and Bay 11 respectively, including association to NF-κB. Bay-11 7082 demonstrated deregulated NF-κB related members of receptor mediated cell death signaling, i.e TRAF2 and TRADD, as well as deregulated members of the NF-κB signaling pathway from the cytoplasmic compartment, i.e RELB, in Raji cells. Comparably NF-κB network analysis of Raji- and DG-75 cells treated with Bay-11 7082 and Raji cells treated with TPCK demonstrated deregulation of NF-κB target genes CD69 and IL8. These data indicates that NF-kB may play a role in overcoming chemoresistance in BL cells with defective classical apoptosis signaling. NF-κB network analysis of Raji- and DG-75 cells treated with Bay-11 7082 and Raji cells treated with TPCK
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