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Links from GEO DataSets

Items: 20

1.

Lamin B1 loss promotes lung cancer development and metastasis by epigenetic derepression of RET [ChIP-Seq]

(Submitter supplied) Although abnormal nuclear structure is an important criterion for cancer diagnostics, remarkably little is known about its relationship to tumor development. Here we report that loss of lamin B1, a determinant of nuclear architecture, plays a key role in lung cancer. We found that lamin B1 levels were reduced in lung cancer patients. Lamin B1 silencing in lung epithelial cells promoted epithelial-mesenchymal transition, cell migration, tumor growth and metastasis. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
8 Samples
Download data: BW
Series
Accession:
GSE94679
ID:
200094679
2.

Lamin B1 loss promotes lung cancer development and metastasis by epigenetic derepression of RET

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL18635 GPL19057
12 Samples
Download data: BW
Series
Accession:
GSE94681
ID:
200094681
3.

Lamin B1 loss promotes lung cancer development and metastasis by epigenetic derepression of RET [RNA-Seq]

(Submitter supplied) Although abnormal nuclear structure is an important criterion for cancer diagnostics, remarkably little is known about its relationship to tumor development. Here we report that loss of lamin B1, a determinant of nuclear architecture, plays a key role in lung cancer. We found that lamin B1 levels were reduced in lung cancer patients. Lamin B1 silencing in lung epithelial cells promoted epithelial-mesenchymal transition, cell migration, tumor growth and metastasis. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18635
4 Samples
Download data: BW, XLSX
Series
Accession:
GSE94680
ID:
200094680
4.

Chip-seq analysis of H3K4me3, H3K27me3, DNMT1 and EZH2 binding to chromatin following acute (10 days) and chronic (10 months) treatment of human bronchial epithelial cells (HBEC3KT) cells with 10 µg/ml cigarette smoke condensate (CSC).

(Submitter supplied) We define how chronic cigarette smoke-induced time-dependent epigenetic alterations can sensitize human bronchial epithelial cells (HBEC) for transformation by a single oncogene. The smoke-induced, chromatin changes include initial repressive polycomb marking of genes later manifesting abnormal DNA methylation by 10 months. At this time, cells manifest epithelial to mesenchymal changes, anchorage-independent growth and upregulated RAS/MAPK signaling with silencing of hyper-methylated genes normally inhibiting these pathways and which are associated with smoking related NSCLC. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
20 Samples
Download data: BED
Series
Accession:
GSE103331
ID:
200103331
5.

Exome-seq analysis of human bronchial epithelial cells (HBEC3KT) cells pre and post treatment with DMSO (Control) or 10 µg/ml cigarette smoke condensate (CSC) for 15 months and tumor xenografts obtained with 15 month CSC treated cells expressing KRASV12

(Submitter supplied) We define how chronic cigarette smoke-induced time-dependent epigenetic alterations can sensitize human bronchial epithelial cells (HBEC) for transformation by a single oncogene. The smoke-induced, chromatin changes include initial repressive polycomb marking of genes later manifesting abnormal DNA methylation by 10 months. At this time, cells manifest epithelial to mesenchymal changes, anchorage-independent growth and upregulated RAS/MAPK signaling with silencing of hyper-methylated genes normally inhibiting these pathways and which are associated with smoking related NSCLC. more...
Organism:
Homo sapiens
Type:
Other
Platforms:
GPL15520 GPL16791
10 Samples
Download data
Series
Accession:
GSE103150
ID:
200103150
6.

Chronic Cigarette Smoke-Induced Epigenomic, gene expression and chromatin changes in Bronchial Epithelial Cells

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array; Expression profiling by array; Other; Genome binding/occupancy profiling by high throughput sequencing
4 related Platforms
86 Samples
Download data: BED, IDAT, PDF, TXT
Series
Accession:
GSE101864
ID:
200101864
7.

Gene Expression of HBEC-3KT cells exposed to cigarette smoke condensate (CSC) over a period of 15 months

(Submitter supplied) We define how chronic cigarette smoke-induced time-dependent epigenetic alterations can sensitize human bronchial epithelial cells (HBEC) for transformation by a single oncogene. The smoke-induced, chromatin changes include initial repressive polycomb marking of genes later manifesting abnormal DNA methylation by 10 months. At this time, cells manifest epithelial to mesenchymal changes, anchorage-independent growth and upregulated RAS/MAPK signaling with silencing of hyper-methylated genes normally inhibiting these pathways and which are associated with smoking related NSCLC. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10332
16 Samples
Download data: PDF, TXT
Series
Accession:
GSE101863
ID:
200101863
8.

Genes expression in xenografts obtained from 15 months cigarette smoke condensate (CSC)-exposed HBEC cells following expression of KRASV12

(Submitter supplied) We define how chronic cigarette smoke-induced time-dependent epigenetic alterations can sensitize human bronchial epithelial cells (HBEC) for transformation by a single oncogene. The smoke-induced, chromatin changes include initial repressive polycomb marking of genes later manifesting abnormal DNA methylation by 10 months. At this time, cells manifest epithelial to mesenchymal changes, anchorage-independent growth and upregulated RAS/MAPK signaling with silencing of hyper-methylated genes normally inhibiting these pathways and which are associated with smoking related NSCLC. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10332
9 Samples
Download data: PDF, TXT
Series
Accession:
GSE101862
ID:
200101862
9.

Methylation analysis of HBEC cells exposed to cigarette smoke condensate (CSC) over a period of 15 months

(Submitter supplied) We define how chronic cigarette smoke-induced time-dependent epigenetic alterations can sensitize human bronchial epithelial cells (HBEC) for transformation by a single oncogene. The smoke-induced, chromatin changes include initial repressive polycomb marking of genes later manifesting abnormal DNA methylation by 10 months. At this time, cells manifest epithelial to mesenchymal changes, anchorage-independent growth and upregulated RAS/MAPK signaling with silencing of hyper-methylated genes normally inhibiting these pathways and which are associated with smoking related NSCLC. more...
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array
Platform:
GPL13534
31 Samples
Download data: IDAT, TXT
Series
Accession:
GSE101673
ID:
200101673
10.

Lamin B1 depletion in senescent cells leads to large-scale changes in the chromatin landscape

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL10999 GPL11154 GPL570
27 Samples
Download data: BW, CEL
Series
Accession:
GSE36641
ID:
200036641
11.

Lamin B1 Depletion in Senescent Cells Triggers Large-Scale Changes in Gene Expression and in the Chromatin Landscape [ expression array ]

(Submitter supplied) Cellular senescence is a stable proliferation arrest in response to stress, associated with an altered secretory pathway (Senescence Associated Secretory Phenotype (SASP)). Senescence-associated proliferation arrest and the SASP are thought to act in concert to promote tumor suppression and tissue aging. While chromatin regulation and down regulation of lamin B1 have been implicated as effectors of cell senescence, functional interactions between them are poorly understood. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
10 Samples
Download data: CEL
Series
Accession:
GSE36640
ID:
200036640
12.

Lamin B1 depletion in senescent cells triggers large-Scale changes in gene expression and in the chromatin landscape[ChIP-seq]

(Submitter supplied) Cellular senescence is a stable proliferation arrest in response to stress, associated with an altered secretory pathway (Senescence Associated Secretory Phenotype (SASP)). Senescence-associated proliferation arrest and the SASP are thought to act in concert to promote tumor suppression and tissue aging. While chromatin regulation and down regulation of lamin B1 have been implicated as effectors of cell senescence, functional interactions between them are poorly understood. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL11154 GPL10999
17 Samples
Download data: BED, BW
Series
Accession:
GSE36616
ID:
200036616
13.

Loss of malignancy of the spontaneous pulmonary metastasis in a human-in-mouse breast cancer model

(Submitter supplied) Patient-derived human-in-mouse breast tumor xenograft models with spontaneous lung metastases1 have emerged as a powerful system to characterize and target cancer metastasis. To evaluate the malignancy of metastatic lesions in the mouse lungs, we implanted the pulmonary metastatic cells into the mouse mammary fat pads. Surprisingly, compared to the parental tumor model, the lung met-derived model showed a slower growth rate and a reduced metastatic potential with a more differentiated epithelial status. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL7504
15 Samples
Download data
Series
Accession:
GSE59750
ID:
200059750
14.

Epigenomic profiling of Non-small-cell Lung Cancer (NSCLC) cells with or without Eed

(Submitter supplied) Polycomb repressive complexes (PRC) are frequently implicated in human cancer acting either as oncogenes or tumor suppressors. Here we show that PRC2 is a critical regulator of Kras-driven non-small-cell lung cancer (NSCLC) progression. Modulation of PRC2 by either Ezh2 overexpression or Eed deletion enhances Kras-driven adenomagenesis and inflammation, respectively. Eed-loss-driven inflammation leads to massive macrophage recruitment and marked decline in tissue function. more...
Organism:
Homo sapiens; Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL13112 GPL17021 GPL16791
31 Samples
Download data: BED, BIGWIG, BW, TXT
Series
Accession:
GSE61190
ID:
200061190
15.

Loss of Lamin A/C in myeloid cells promotes lung metastasis through Gfi-1 and C/EBPe-mediated granulocytic differentiation

(Submitter supplied) The immune suppressive tumor microenvironment contributes to metastatic spread. In particular, tumor-associated myeloid cells, which differ from normal myeloid cells, suppress cytotoxic T lymphocyte-mediated anti-tumor immunity. However, the underlying molecular mechanisms for tumor-associated myeloid lineage differentiation and functional properties are not well understood. Here we report a lack of Lamin A/C, a nuclear lamina protein associated with chromatin remodeling, in tumor-associated granulocytic myeloid cells. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
8 Samples
Download data: TXT
Series
Accession:
GSE141124
ID:
200141124
16.

Protein kinase A-mediated phosphorylation regulates STAT3 activation and oncogenic EZH2 activity

(Submitter supplied) The effect of T372E-EZH2 and Wt-EZH2 overexpression on gene expression in TOV112D cells. We found in this study that Protein Kinase A phosphorylates T372-EZH2 and wanted to determine the gene expression changes brought upon this phosphorylation. We made a point mutation (T372E) that mimicked phospho T372-EZH2. The objective was to observe transcriptional changes in TOV112D cells in response to ectopic expression of Wt-EZH2 and T372E-EZH2 point mutation in TOV112D cells.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
8 Samples
Download data: TXT, XLSX
17.

Genome-wide Mapping of Lamin B1 Reveals the Existence of Dynamic and Functional Euchromatin Lamin B1 Domains (eLADs) at the onset of the Epithelial to Mesenchymal Transition

(Submitter supplied) Lamins (A/C and B) are type V intermediate filaments and constitute the major cytoskeleton component of nuclei. They are assembled forming a filamentous meshwork that is mainly located between the inner nuclear membrane and the peripheral chromatin in where they form structural and conserved elements called lamin-associated domains (LADs) that cover around 40% of the mammalian genome. However, a small fraction of lamins are also located in the nucleoplasm although is still unclear if represents a fraction that is in transit towards the nuclear membrane, a reservoir for protein turnover or they have specific functions in nuclear organization6. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Other
Platforms:
GPL17021 GPL13112
27 Samples
Download data: BED, BEDGRAPH, TAR, TXT
Series
Accession:
GSE96033
ID:
200096033
18.

Epigenetic reprogramming in hepatic carcinogenesis

(Submitter supplied) Genomic sequencing of hepatocellular carcinoma (HCC) uncovers a paucity of actionable mutations, underscoring the necessity to exploit epigenetic vulnerabilities for therapeutics. In HCC, EZH2-mediated H3K27me3 represents a major oncogenic chromatin modification, but how it modulates the therapeutic vulnerability of signaling pathways remains unknown. Here, we identified that EZH2 maintains H3K27 methylome through epigenetic silencing of specific gene sets. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18480
10 Samples
Download data: BW
Series
Accession:
GSE113326
ID:
200113326
19.

Sox4 is a master regulator of epithelial-mesenchymal transition (EMT) by controlling Ezh2 expression and epigenetic reprogramming

(Submitter supplied) Gene expression profiling has uncovered the transcription factor Sox4 with up-regulated activity during TGFβ-induced EMT in normal and cancerous breast epithelial cells. Sox4 is indispensable for EMT and cell survival in vitro and for primary tumor growth and metastasis in vivo. Among several EMT-relevant genes, Sox4 directly regulates the expression of Ezh2, encoding the Polycomb group histone methyltransferase that trimethylates histone 3 lysine 27 (H3K27me3) for gene repression. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL9250
13 Samples
Download data: BED
Series
Accession:
GSE45579
ID:
200045579
20.

Expression data from Sox4 knockdown cells in the presence and absence of TGFβ in NMuMG cells

(Submitter supplied) Expression profiling after Sox4 knockdown (KD) during epithelial to mesenchymal transition (EMT) in NMuMG reveals a significant number of genes that are transcriptionally deregulated.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
8 Samples
Download data: CEL
Series
Accession:
GSE44050
ID:
200044050
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