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Affymetrix SNP array data for oral squamous cell carcinoma samples

ABSTRACT: The development of oral squamous cell carcinoma (OSCC) is a multistep process requiring the accumulation of genetic alterations. To identify genes responsible for OSCC development, we performed high-density single-nucleotide polymorphism array analysis and genome-wide gene expression profiling on OSCC tumors. These analyses identified "absent in melanoma (AIM2)" and "interferon-inducible gene 16 (IFI16)," mapped to the hematopoietic IFN-inducible nuclear proteins with 200-amino acid repeat (HIN-200) gene cluster in the amplified region of chromosome 1q23, with overexpression in OSCCs. AIM2 and IFI16 are cytoplasmic double-stranded DNA sensors for innate immunity and act as tumor suppressors in several human cancers. Knockdown of AIM2 or IFI16 in OSCC cells resulted in the suppression of cell growth and the induction of apoptosis, accompanied by the downregulation of NF-κB activation. Because all of the OSCC cell lines had impairment of p53 activity, wild-type p53 was introduced in p53-deficient OSCC cells, and as a result, the expression of wild-type p53 suppressed cell growth and induced apoptosis via suppression of NF-κB activity. Finally, the coexpression of AIM2 and IFI16 significantly enhanced cell growth in p53-deficient cells; in contrast, the expression of AIM2 and/or IFI16 in cells bearing wild-type p53 suppressed cell growth. Moreover, AIM2 and IFI16 synergistically enhanced NF-κB signaling in p53-deficient cells. Thus, expression of AIM2 and IFI16 may have oncogenic functions in OSCC cells inactivating p53 system.

ORGANISM(S): Homo sapiens

PROVIDER: GSE34507 | GEO | 2011/12/30

SECONDARY ACCESSION(S): PRJNA151301

REPOSITORIES: GEO

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Affymetrix SNP array data for oral squamous cell carcinoma samples

Project description:The development of oral squamous cell carcinoma (OSCC) is a multistep process requiring the accumulation of genetic alterations. To identify genes responsible for OSCC development, we performed high-density single-nucleotide polymorphism array analysis and genome-wide gene expression profiling on OSCC tumors. These analyses identified "absent in melanoma (AIM2)" and "interferon-inducible gene 16 (IFI16)," mapped to the hematopoietic IFN-inducible nuclear proteins with 200-amino acid repeat (HIN-200) gene cluster in the amplified region of chromosome 1q23, with overexpression in OSCCs. AIM2 and IFI16 are cytoplasmic double-stranded DNA sensors for innate immunity and act as tumor suppressors in several human cancers. Knockdown of AIM2 or IFI16 in OSCC cells resulted in the suppression of cell growth and the induction of apoptosis, accompanied by the downregulation of NF-κB activation. Because all of the OSCC cell lines had impairment of p53 activity, wild-type p53 was introduced in p53-deficient OSCC cells, and as a result, the expression of wild-type p53 suppressed cell growth and induced apoptosis via suppression of NF-κB activity. Finally, the coexpression of AIM2 and IFI16 significantly enhanced cell growth in p53-deficient cells; in contrast, the expression of AIM2 and/or IFI16 in cells bearing wild-type p53 suppressed cell growth. Moreover, AIM2 and IFI16 synergistically enhanced NF-κB signaling in p53-deficient cells. Thus, expression of AIM2 and IFI16 may have oncogenic functions in OSCC cells inactivating p53 system. Copy number analysis of Affymetrix 250K SNP arrays was performed for 5 oral leukoplakia samples, 20 oral squamous cell carcinoma samples, and 8 oral squamous cell carcinoma cell lines.

2011-12-30 | E-GEOD-34507 | biostudies-arrayexpress

The function and mechanism about how ORAOV1-B potentiates the OSCC metastasis.

Project description:Lymph node metastasis, a powerful prognostic indicator of oral squamous cell carcinoma (OSCC), is chiefly responsible for cancer death. Long non-coding RNA (lncRNA) is recently addressed to significantly account for modulating OSCC metastasis. Here, we identified a novel alternative splice of Oral Cancer Overexpressed 1 (ORAOV1), ORAOV1-B, which was subsequently validated as an lncRNA and correlated with OSCC lymph node metastasis; significantly increased invasion and migration were observed in ORAOV1-B-overexpressed OSCC cells; In the metastatic model, ORAOV1-B also significantly contributed to OSCC-related lung metastasis. cDNA microarrays was performed to compare up- or down-regulated genes in EV and ORAOV1-B sets of OSCC, which suggested TNFα as a potential downstream of ORAOV1-B and the upregulation of pro-inflammatory genes, indicating the activation of NF-κB pathway. In summary, the novel splice variant ORAOV1-B is an lncRNA, which significantly potentiates OSCC invasion and metastasis by binding to Hsp90 and activating the NF-κB-TNFα loop. Our study implies that ORAOV1-B might serve as an attractive OSCC metastasis intervention target.

2020-03-04 | GSE145599 | GEO

Critical role for the DNA receptor AIM2 in stem-cell proliferation and cancer

Project description:Colorectal cancer is a leading cause of cancer-related deaths. Mutations in the innate immune receptor AIM2 are frequently identified in patients with colorectal cancer, but how AIM2 modulates colonic tumorigenesis is unknown. Here, we found that Aim2-deficient mice were hypersusceptible to colonic tumor development. Production of inflammasome-associated cytokines and other inflammatory mediators were largely intact in Aim2-deficient mice, however, intestinal stem cells were prone to uncontrolled proliferation. Aberrant Wnt signaling expanded a population of tumor-initiating stem cells in the absence of AIM2. Susceptibility of Aim2-deficient mice to colorectal tumorigenesis was enhanced by a dysbiotic gut microbiota, which was reduced by reciprocal exchange of gut microbiota with wild-type healthy mice. These findings uncover a synergy between a specific host genetic factor and gut microbiota in determining the susceptibility to colorectal cancer. Therapeutic modulation of AIM2 expression and microbiota has the potential to prevent colorectal cancer. We used microarrays to compare the transcriptome Aim2 deficent mice to wild type mice in colon tumor and colitis samples. Here were 12 mice in total, 3 for each genotype and tissue combination.

2015-07-15 | E-GEOD-69436 | biostudies-arrayexpress

p100 deficiency alone is insufficient for full activation of the alternative NF-κB pathway: TNF signaling cooperates with p52-RelB activation in the transcriptional regulation of the enpp2/autotaxin promoter

Project description:Background: Constitutive activation of the alternative NF-κB pathway leads to marginal zone B cell expansion and disorganized spleen microarchitecture. Furthermore, uncontrolled alternative NF-κB signaling results in the development and progression of cancer. We aimed here to learn about the mechanisms how does the constitutively active alternative NF-κB pathway exert its effects in these malignant processes. Methodology/Principal Findings: To explore the consequences of constitutive alternative NF-κB activation on genome-wide transcription, we compared gene expression profiles of wild-type and NF-kB2/p100-deficient (p100-/-) primary mouse embryonic fibroblasts (MEFs) and spleens. Microarray experiments revealed 73 differentially regulated genes in p100-/- vs. wild-type MEFs. Chromatin immunoprecipitation (ChIP) assays showed in p100-/- MEFs direct binding of RelB and p52 to the promoter of the enpp2 gene encoding Enpp2/Autotaxin, a protein with an important role in lymphocyte homing and cell migration. Gene ontology analysis revealed upregulation of genes with anti-apoptotic/proliferative activity (enpp2, serpina3g, traf1, rrad), chemotactic/locomotory activity (enpp2, ccl8), and lymphocyte homing activity (enpp2, cd34). Most importantly, biochemical analyses of MEFs and gene expression analyses of mice indicated a crosstalk between classical and alternative NF-κB pathways. Conclusions/Significance: The present results show that uncontrolled alternative NF-κB signaling is further enhanced by classical NF-κB activation, indicating that p100 deficiency alone is insufficient for full induction of a subset of genes by the alternative NF-κB pathway.

2012-12-21 | GSE30317 | GEO

Genome-wide chromatin profiles of PBRM1 Drug treatment [RNA-Seq]

Project description:PBRM1 encodes an accessory subunit of the PBAF subclass of the SWI/SNF chromatin remodeler and the inactivation of PBRM1 is the second most frequent mutational event in kidney cancer. However, the impact of PBRM1 loss on chromatin remodeling, especially pertaining to kidney tumorigenesis, has not been well examined. Here we show that in VHL-deficient renal tumors, PBRM1 deficiency results in aberrant PBAF complexes that localize to de novo genomic loci and activate the pro-tumorigenic NF-κB pathway. PBRM1-deficient PBAF complexes, despite retaining the association between SMARCA4 and ARID2, have loosely tethered BRD7 and redistribute from promoter proximal regions to distal enhancers containing NF-κB motifs. Subsequently, PBRM1-deficient cells display heightened NF-κB activity in multiple models and clinical samples. The ATPase function of SMARCA4 maintains chromatin occupancy of both pre-existing and newly acquired RELA specific to PBRM1 loss, and activates downstream target gene expression. Proteasome inhibitor bortezomib reverses NF-κB activation by reducing RELA occupancy and delays growth of PBRM1-deficient tumors. In conclusion, PBRM1 safeguards the chromatin by repressing aberrant liberation of pro-tumorigenic NF-κB target genes by residual PBRM1-deficient PBAF complexes.

2023-02-13 | GSE222245 | GEO

Genome-wide chromatin profiles of PBRM1 Drug treatment [ChIP-Seq]

2023-02-13 | GSE222244 | GEO

Critical role for the DNA receptor AIM2 in stem-cell proliferation and cancer

2015-07-15 | GSE69436 | GEO

Downregulation of LATS kinases alters p53 to promote cell migration

Project description:p53 is a pivotal tumor suppressor and a major barrier against cancer. We now report that silencing of the Hippo pathway tumor suppressors LATS1 and LATS2 in non-transformed mammary epithelial cells reduces p53 phosphorylation and increases its association with the p52 NF-κB subunit. Moreover, it partly shifts p53’s conformation and transcriptional output towards a state resembling cancer-associated p53 mutants, and endow p53 with the ability to promote cell migration. Notably, LATS1 and LATS2 are frequently downregulated in breast cancer; we propose that such downregulation might benefit cancer by converting p53 from a tumor suppressor into a tumor facilitator.

2018-10-25 | PXD003120 | Pride

Interactome analysis of PYHIN immune regulators

Project description:The human PYHIN proteins, AIM2, IFI16, IFIX, and MNDA, are regulators of immune response, transcription, apoptosis, and cell cycle. However, their protein interactions and underlying mechanisms remain largely uncharacterized. Here, we provide the interaction network for all PYHIN proteins. By designing a cell-based inducible system and integrating microscopy, immunoaffinity capture, quantitative mass spectrometry, and bioinformatics, we identified over 300 PYHIN interactions reflective of diverse functions.

2015-03-12 | PXD001572 | Pride

Rad21-mediated NF-κB signaling limits hematopoietic stem cell self-renewal in aging and inflammation

Project description:MTD project_description Inflammation and decreased stem cell function characterize organism aging, yet the relationship between these factors remains incompletely understood. This study shows that aged hematopoietic stem and progenitor cells exhibit increased ground-stage NF-κB activity, which enhances their responsiveness to undergo differentiation and loss of self-renewal in response to inflammation. The study identifies Rad21/cohesin as a critical mediator of NF-κB signals, by increasing chromatin accessibility of inter-/intra-genic and enhancer regions. Rad21/NF-κB are required for normal differentiation, but limit self-renewal of hematopoietic stem cells (HSCs) during aging and inflammation in an NF-κB dependent manner. HSCs from aged mice fail to downregulate Rad21/cohesin and inflammation/differentiation inducing signals in the resolution phase after acute inflammation. and The inhibition of cohesin/NF-κB is sufficient to revert the hypersensitivity of aged HSPCs to inflammation-induced differentiation. During aging, myeloid-biased HSCs with disrupted and naturally occurring reduced expression of Rad21/cohesin are increasingly selected over lymphoid-biased HSCs. Together, Rad21/cohesin mediated NF-κB signaling limits HSPC function during aging and selects for cohesin deficient HSCs with myeloid skewed differentiation.

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