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Latent Membrane Protein 1 and macrophage-derived TNFα synergistically activate and mobilize invadopodia to drive invasion of nasopharyngeal carcinoma

ABSTRACT: To investigate the effect of TNFα and EBV on invadopodia formation, we treated the EBV-positive and -negative NPC43 cells seeded on gelatin with or without TNFα We then performed gene expression profiling analysis using data obtained from RNA-seq of 4 different groups

ORGANISM(S): Homo sapiens

PROVIDER: GSE218167 | GEO | 2022/11/22

REPOSITORIES: GEO

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Latent Membrane Protein 1 and macrophage-derived TNFα synergistically activate and mobilize invadopodia to drive invasion of nasopharyngeal carcinoma

Project description:Latent Membrane Protein 1 and macrophage-derived TNFα synergistically activate and mobilize invadopodia to drive invasion of nasopharyngeal carcinoma

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Latent membrane protein 1 and macrophage-derived TNFα synergistically activate and mobilize invadopodia to drive invasion of nasopharyngeal carcinoma.

Project description:Invadopodia are actin-rich membrane protrusions that digest the matrix barrier during cancer metastasis. Since the discovery of invadopodia, they have been visualized as localized and dot-like structures in different types of cancer cells on top of a 2D matrix. In this investigation of Epstein-Barr virus (EBV)-associated nasopharyngeal carcinoma (NPC), a highly invasive cancer frequently accompanied by neck lymph node and distal organ metastases, we revealed a new form of invadopodium with mobilizing features. Integration of live-cell imaging and molecular assays revealed the interaction of macrophage-released TNFα and EBV-encoded latent membrane protein 1 (LMP1) in co-activating the EGFR/Src/ERK/cortactin and Cdc42/N-WASP signaling axes for mobilizing the invadopodia with lateral movements. This phenomenon endows the invadopodia with massive degradative power, visualized as a shift of focal dot-like digestion patterns on a 2D gelatin to a dendrite-like digestion pattern. Notably, single stimulation of either LMP1 or TNFα could only enhance the number of ordinary dot-like invadopodia, suggesting that the EBV infection sensitizes the NPC cells to form mobilizing invadopodia when encountering a TNFα-rich tumor microenvironment. This study unveils the interplay of EBV and stromal components in driving the invasive potential of NPC via unleashing the propulsion of invadopodia in overcoming matrix hurdles. © 2022 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.

| S-EPMC10108171 | biostudies-literature

Control, TNFα and TNFα+JNK I treated GSCs

Project description:Control, TNFα and TNFα+JNK I treated GSCs

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TNFα Signaling Exposes Latent Estrogen Receptor Binding Sites in Breast Cancer Cells [GRO-seq]

Project description:The interplay between mitogenic and proinflammatory signaling pathways play key roles in determining the phenotypes and clinical outcomes of breast cancers. We have used global nuclear run-on coupled with deep sequencing to characterize the immediate transcriptional responses of MCF-7 breast cancer cells treated with estradiol, TNFα, or both. In addition, we have integrated these data with chromatin immunoprecipitation coupled with deep sequencing for estrogen receptor alpha (ERα), the pioneer factor FoxA1 and the p65 subunit of the NF-κB transcription factor. Our results indicate extensive transcriptional interplay between these two signaling pathways, which is observed for a number of classical mitogenic and proinflammatory protein-coding genes. In addition, GRO-seq has allowed us to capture the transcriptional crosstalk at the genomic locations encoding for long non-coding RNAs, a poorly characterized class of RNAs which have been shown to play important roles in cancer outcomes. The synergistic and antagonistic interplay between estrogen and TNFα signaling at the gene level is also evident in the patterns of ERα and NF-κB binding, which relocalize to new binding sites that are not occupied by either treatment alone. Interestingly, the chromatin accessibility of classical ERα binding sites is predetermined prior to estrogen treatment, whereas ERα binding sites gained upon co-treatment with TNFα require NF-κB and FoxA1 to promote chromatin accessibility de novo. Our data suggest that TNFα signaling recruits FoxA1 and NF-κB to latent ERα enhancer locations and directly impact ERα enhancer accessibility. Binding of ERα to latent enhancers upon co-treatment, results in increased enhancer transcription, target gene expression and altered cellular response. This provides a mechanistic framework for understanding the molecular basis for integration of mitogenic and proinflammatory signaling in breast cancer.

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Transcriptome analysis of IEC4.1 cells in response to TNFα stimulation.

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Expression data from EBV-encoded latent membrane protein 2A (LMP2A) positive and negative nasopharyngeal carcinoma (NPC) cell lines

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2018-08-21 | GSE118807 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of control, TNFα and TNFα+JNK I treated GSCs Transcriptomes

Project description:Among 830 TNFα-induced genes (at least 1.5 folds of upregulation in TNFα-treated TPC2-4 cells compared with control), the expression of 268 genes is significantly suppressed by JNKi treatment (TPC2-4 TNFα+JNKi/TPC2-4 TNFα, JNKi: JNK-IN-8, a kinase inhibitor specific for JNK (c-Jun N-terminal kinase) that inhibited phosphorylation of c-JUN)

2022-08-24 | GSE194220 | GEO

ATAC-seq comparatively analyse chromatin accessibility varition of control, TNFα and TNFα+JNK I treated GSCs

Project description:Among 3,673 TNFα-induced gain of accessibility (at least 2 folds of upregulation in TNFα-treated TPC2-4 cells compared with control), and most of the gained peaks were significantly suppressed by JNKi treatment (TPC2-4 TNFα+JNKi/TPC2-4 TNFα, JNKi: JNK-IN-8, a kinase inhibitor specific for JNK (c-Jun N-terminal kinase) that inhibited phosphorylation of c-JUN)

2022-08-24 | GSE194221 | GEO

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Project description:TNFα is a cytokine with multiple biological effects. It activates cascading signal pathways by binding to receptors on the cell membrane, regulating processes such as cell growth, differentiation, apoptosis, and inflammatory responses. The formation of skeletal muscle primarily relies on processes such as myoblasts proliferation, migration, differentiation, cytoskeletal rearrangement, and myotube fusion, which constitute a complex and coordinated process regulated by multiple genes. While research on TNFα has primarily focused on immunology, some studies suggest that TNFα also plays a physiological role in myogenesis, muscle repair, diseases, and atrophy.We isolated the nuclei (N) and cytoplasm (C) of flox and TNFα-CKO primary myoblasts in the early stages of differentiation and attempted to identify new targets in the TNFα signaling pathway.

2024-08-09 | PXD046525 | Pride

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Project description:To characterize the transcriptome of primary vascular endothelial cells (ECs) during TNFα-response, we performed total RNA-seq on primary human aortic ECs (HAEC), before and after TNFα (45 min. 10 ng/mL).

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