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CDYL2 epigenetically regulates MIR124 to control NF-kB/STAT3-dependent breast cancer cell plasticity

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE150320 | GEO | 2020/05/16

REPOSITORIES: GEO

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CDYL2 Epigenetically Regulates MIR124 to Control NF-κB/STAT3-Dependent Breast Cancer Cell Plasticity.

Project description:Epigenetic deregulation of gene transcription is central to cancer cell plasticity and malignant progression but remains poorly understood. We found that the uncharacterized epigenetic factor chromodomain on Y-like 2 (CDYL2) is commonly over-expressed in breast cancer, and that high CDYL2 levels correlate with poor prognosis. Supporting a functional role for CDYL2 in malignancy, it positively regulated breast cancer cell migration, invasion, stem-like phenotypes, and epithelial-to-mesenchymal transition. CDYL2 regulation of these plasticity-associated processes depended on signaling via p65/NF-κB and STAT3. This, in turn, was downstream of CDYL2 regulation of MIR124 gene transcription. CDYL2 co-immunoprecipitated with G9a/EHMT2 and GLP/EHMT1 and regulated the chromatin enrichment of G9a and EZH2 at MIR124 genes. We propose that CDYL2 contributes to poor prognosis in breast cancer by recruiting G9a and EZH2 to epigenetically repress MIR124 genes, thereby promoting NF-κB and STAT3 signaling, as well as downstream cancer cell plasticity and malignant progression.

| S-EPMC7251929 | biostudies-literature

CDYL2 epigenetically regulates MIR124 to control NF-kB/STAT3-dependent breast cancer cell plasticity [RNA-seq]

Project description:Epigenetic deregulation of gene transcription is central to cancer cell plasticity and malignant progression, but remains poorly understood. We found that the uncharacterized epigenetic factor Chromodomain on Y-like 2 (CDYL2) is commonly over-expressed in breast cancer, and that high CDYL2 levels correlate with poor prognosis. Supporting a functional role for CDYL2 in malignancy, it positively regulated breast cancer cell migration, invasion, stem-like phenotypes, and epithelial-to-mesenchymal transition (EMT). CDYL2 regulation of these plasticity-associated processes depended on signaling via p65/NF-kB and STAT3. This, in turn, was downstream of CDYL2 regulation of MIR124 gene transcription. CDYL2 co-immunoprecipitated with G9a/EHMT2 and GLP/EHMT1, and regulated the chromatin enrichment of G9a and EZH2 at MIR124 genes. We propose that CDYL2 contributes to poor prognosis in breast cancer by recruiting G9a and EZH2 to epigenetically repress MIR124 genes, thereby promoting NF-kB and STAT3 signaling, as well as downstream cancer cell plasticity and malignant progression.

2020-05-17 | GSE150306 | GEO

CDYL2 epigenetically regulates MIR124 to control NF-kB/STAT3-dependent breast cancer cell plasticity [ChIP-seq]

2020-05-17 | GSE150274 | GEO

CDYL2 epigenetically regulates MIR124 to control NF-kB/STAT3-dependent breast cancer cell plasticity [MDA-MB-231 RNA-seq]

2020-05-17 | GSE150319 | GEO

CDYL2 epigenetically regulates MIR124 to control NF-kB/STAT3-dependent breast cancer cell plasticity

Project description:CDYL2 epigenetically regulates MIR124 to control NF-kB/STAT3-dependent breast cancer cell plasticity

| PRJNA631761 | ENA

CDYL2 epigenetically regulates MIR124 to control NF-kB/STAT3-dependent breast cancer cell plasticity [ChIP-seq]

Project description:CDYL2 epigenetically regulates MIR124 to control NF-kB/STAT3-dependent breast cancer cell plasticity [ChIP-seq]

| PRJNA631707 | ENA

CDYL2 epigenetically regulates MIR124 to control NF-kB/STAT3-dependent breast cancer cell plasticity [RNA-seq]

Project description:CDYL2 epigenetically regulates MIR124 to control NF-kB/STAT3-dependent breast cancer cell plasticity [RNA-seq]

| PRJNA631744 | ENA

CDYL2 epigenetically regulates MIR124 to control NF-kB/STAT3-dependent breast cancer cell plasticity [MDA-MB-231 RNA-seq]

Project description:CDYL2 epigenetically regulates MIR124 to control NF-kB/STAT3-dependent breast cancer cell plasticity [MDA-MB-231 RNA-seq]

| PRJNA631763 | ENA

NF-kB-dependent activation of STAT3 by H. pylori is suppressed by TFF1.

Project description:BackgroundH. pylori infection is the main risk factor for gastric cancer. In this study, we investigated H. pylori-mediated activation of STAT3 and NF-κB in gastric cancer, using in vitro and in vivo models.MethodsTo investigate the activation of NF-κB and STAT3 by H. pylori strains we used in vitro and in vivo mouse models, western blots, immunofluorescence, ChIP Assay, luciferase and quantitative real-time PCR assays.ResultsFollowing infection with H. pylori in vitro, we found an earlier phosphorylation of NF-kB-p65 (S536), followed by STAT3 (Y705). Immunofluorescence, using in vitro and in vivo models, demonstrated nuclear localization of NF-kB and STAT3, following H. pylori infection. NF-kB and STAT3 luciferase reporter assays confirmed earlier activation of NF-kB followed by STAT3. In vitro and in vivo models demonstrated induction of mRNA expression of IL-6 (p < 0.001), VEGF-α (p < 0.05), IL-17 (p < 0.001), and IL-23 (p < 0.001). Using ChIP, we confirmed co-binding of both NF-kB-p65 and STAT3 on the IL6 promoter. The reconstitution of Trefoil Factor 1 (TFF1) suppressed activation of NF-kB with reduction in IL6 levels and STAT3 activity, in response to H. pylori infection. Using pharmacologic (BAY11-7082) and genetic (IκB super repressor (IκBSR)) inhibitors of NF-kB-p65, we confirmed the requirement of NF-kB-p65 for activation of STAT3, as measured by phosphorylation, transcription activity, and nuclear localization of STAT3 in in vitro and in vivo models.ConclusionOur findings suggest the presence of an early autocrine NF-kB-dependent activation of STAT3 in response to H. pylori infection. TFF1 acts as an anti-inflammatory guard against H. pylori-mediated activation of pro-inflammatory networks.

| S-EPMC8380333 | biostudies-literature

KDM6A epigenetically regulates subtype plasticity in small cell lung cancer.

Project description:Small cell lung cancer (SCLC) exists broadly in four molecular subtypes: ASCL1, NEUROD1, POU2F3 and Inflammatory. Initially, SCLC subtypes were thought to be mutually exclusive, but recent evidence shows intra-tumoural subtype heterogeneity and plasticity between subtypes. Here, using a CRISPR-based autochthonous SCLC genetically engineered mouse model to study the consequences of KDM6A/UTX inactivation, we show that KDM6A inactivation induced plasticity from ASCL1 to NEUROD1 resulting in SCLC tumours that express both ASCL1 and NEUROD1. Mechanistically, KDM6A normally maintains an active chromatin state that favours the ASCL1 subtype with its loss decreasing H3K4me1 and increasing H3K27me3 at enhancers of neuroendocrine genes leading to a cell state that is primed for ASCL1-to-NEUROD1 subtype switching. This work identifies KDM6A as an epigenetic regulator that controls ASCL1 to NEUROD1 subtype plasticity and provides an autochthonous SCLC genetically engineered mouse model to model ASCL1 and NEUROD1 subtype heterogeneity and plasticity, which is found in 35-40% of human SCLCs.

| S-EPMC10546329 | biostudies-literature

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