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Links from GEO DataSets

Items: 20

1.

SPOP mutations derived from prostate cancer establish a DNA hypermethylation epigenome through stabilizing GLP histone methyltransferase [methylation array]

(Submitter supplied) Abnormal DNA methylation is one of the major factors driving oncogenesis and therapy resistance in cancer. The CULLIN3-RBX1 E3 ubiquitin ligase adaptor gene SPOP is the most frequently mutated gene in primary prostate cancers (PCa). SPOP-mutated prostate tumors strikingly associate with strongly elevated levels of genome-wide DNA hypermethylation, although the underlying mechanism remains elusive.We use Illumina Infinium MethylationEPIC BeadChip to depict DNA methylation in control and SPOP F102C stabily expressed 22Rv1 cells. more...
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array
Platform:
GPL23976
8 Samples
Download data: IDAT, TSV
Series
Accession:
GSE179234
ID:
200179234
2.

SPOP mutations derived from prostate cancer establish a DNA hypermethylation epigenome through stabilizing GLP histone methyltransferase

(Submitter supplied) Abnormal DNA methylation is one of the major factors driving oncogenesis and therapy resistance in cancer. The CULLIN3-RBX1 E3 ubiquitin ligase adaptor gene SPOP is the most frequently mutated gene in primary prostate cancers (PCa). SPOP-mutated prostate tumors strikingly associate with strongly elevated levels of genome-wide DNA hypermethylation, although the underlying mechanism remains elusive. We use reduced representation bisulfite sequencing (RRBS) to depict DNA methylation in control and SPOP F133V stably expressed 22Rv1 cells. more...
Organism:
Homo sapiens
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL20301
4 Samples
Download data: TXT
Series
Accession:
GSE155491
ID:
200155491
3.

G3BP1 inhibits Cul3SPOP to amplify AR signaling and promote prostate tumorigenesis

(Submitter supplied) Speckle-type POZ protein (SPOP), an E3 ubiquitin ligase, acts as a tumor suppressor. We identified G3BP1 as non-substrate interactor of SPOP. G3BP1 is a well-known oncogene in many cancer types, but its role in prostate cancer (PCa) remains largely elusive. We showed that G3BP1 functions as an upstream regulator and potent endogenous inhibitor of Cul3SPOP, suggesting a distinctive Cul3SPOP inactivation independent of SPOP mutations. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
9 Samples
Download data: TXT
4.

SPOP mutation confers intrinsic BET inhibitor resistance in prostate cancer (BRDs_OE_RNA-seq)

(Submitter supplied) Bromodomain and extraterminal domain (BET) protein inhibitors are emerging as promising therapeutics of cancers including prostate cancer. The E3 ubiquitin ligase adaptor protein speckle-type POZ protein (SPOP) is implicated in human prostate cancers due to its frequent mutation. Here we demonstrate that SPOP binds to the BET proteins BRD2, BRD3 and BRD4. Wild-type SPOP, but not prostate cancer-associated mutants, promotes polyubiquitination and proteasome degradation of BET proteins by recognizing a common degron motif. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
4 Samples
Download data: TXT
5.

SPOP mutation confers intrinsic BET inhibitor resistance in prostate cancer

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
26 Samples
Download data: BIGWIG, BW, TXT
Series
Accession:
GSE88872
ID:
200088872
6.

SPOP mutation confers intrinsic BET inhibitor resistance in prostate cancer (ChIP-Seq)

(Submitter supplied) Bromodomain and extraterminal domain (BET) protein inhibitors are emerging as promising therapeutics of cancers including prostate cancer. The E3 ubiquitin ligase adaptor protein speckle-type POZ protein (SPOP) is implicated in human prostate cancers due to its frequent mutation. Here we demonstrate that SPOP binds to the BET proteins BRD2, BRD3 and BRD4. Wild-type SPOP, but not prostate cancer-associated mutants, promotes polyubiquitination and proteasome degradation of BET proteins by recognizing a common degron motif. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
10 Samples
Download data: BIGWIG
Series
Accession:
GSE88871
ID:
200088871
7.

SPOP mutation confers intrinsic BET inhibitor resistance in prostate cancer (BRD4_JQ1_RNA-seq)

(Submitter supplied) Bromodomain and extraterminal domain (BET) protein inhibitors are emerging as promising therapeutics of cancers including prostate cancer. The E3 ubiquitin ligase adaptor protein speckle-type POZ protein (SPOP) is implicated in human prostate cancers due to its frequent mutation. Here we demonstrate that SPOP binds to the BET proteins BRD2, BRD3 and BRD4. Wild-type SPOP, but not prostate cancer-associated mutants, promotes polyubiquitination and proteasome degradation of BET proteins by recognizing a common degron motif. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
12 Samples
Download data: BW
8.

Targeting aberrant DNA methylation in mesenchymal stromal cells as a treatment for myeloma bone disease

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Methylation profiling by array; Expression profiling by array
Platforms:
GPL21145 GPL6244
93 Samples
Download data: CEL
Series
Accession:
GSE137419
ID:
200137419
9.

Targeting aberrant DNA methylation in mesenchymal stromal cells as a treatment for myeloma bone disease [methylation II]

(Submitter supplied) Genome wide DNA methylation profiling of bone marrow-derived mesenchymal stromal cells from healthy donors (n=11), monoclonal gammopathy of undetermined significance (MGUS) (n=10), smoldering myeloma (SMM) (n=8), multiple myeloma (MM) (n=9) patients, and healthy donors exposed to the MM.1S cell line (n=3). The Illumina Infinium MethylationEPIC Beadchip was used to obtain DNA methylation profiles across approximately 850,000 CpGs in this cell type.
Organism:
Homo sapiens
Type:
Methylation profiling by array
Platform:
GPL21145
35 Samples
Download data
Series
Accession:
GSE137416
ID:
200137416
10.

Targeting aberrant DNA methylation in mesenchymal stromal cells as a treatment for myeloma bone disease [expression]

(Submitter supplied) Gene expression profiling of bone marrow-derived mesenchymal stromal cells from healthy donors (n=8), monoclonal gammopathy of undetermined significance (MGUS) (n=10), smoldering myeloma (SMM) (n=10) and multiple myeloma (MM) (n=24) patients. Gene expression profile of MSCs was obtained using high density oligonucleotide microarrays (Human Gene 1.0 ST Array from Affymetrix).
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
52 Samples
Download data: CEL
Series
Accession:
GSE137369
ID:
200137369
11.

Targeting aberrant DNA methylation in mesenchymal stromal cells as a treatment for myeloma bone disease [methylation]

(Submitter supplied) Genome wide DNA methylation profiling of bone marrow-derived mesenchymal stromal cells from healthy donors (n=11), monoclonal gammopathy of undetermined significance (MGUS) (n=10), smoldering myeloma (SMM) (n=8), multiple myeloma (MM) (n=9) patients, and healthy donors exposed to the MM.1S cell line (n=3). The Illumina Infinium MethylationEPIC Beadchip was used to obtain DNA methylation profiles across approximately 850,000 CpGs in this cell type.
Organism:
Homo sapiens
Type:
Methylation profiling by array
Platform:
GPL21145
6 Samples
Download data: TXT
Series
Accession:
GSE137360
ID:
200137360
12.

The SPOP-containing Complex Functions as an E3 Ligase for SETD2 to Regulate Gene-Specific H3K36me3-Coupled Alternative Splicing

(Submitter supplied) H3K36me3 has been reported to associate with active gene expression, and SETD2 is the mainly methyltransferase for H3K36me3. We identified SPOP which is a CUL3 family protein as a E3 ligase for SETD2. Genome wide analysis by using ChIPSeq and RNASeq demonstrate that SPOP specificly eliminate H3K36me3 modification at target genes and resulted in alternative splicing of those target genes.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL16791 GPL20301
18 Samples
Download data: TXT, WIG
13.

TRIM28 protects TRIM24 from SPOP-mediated degradation and promotes prostate cancer progression

(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:
GPL15456 GPL10558
27 Samples
Download data: BEDGRAPH, TXT
Series
Accession:
GSE108146
ID:
200108146
14.

TRIM28 protects TRIM24 from SPOP-mediated degradation and promotes prostate cancer progression [microarray]

(Submitter supplied) In this study, proteomic profiling of TRIM24 interactome in conjunction with shRNA screening of TRIM24 top-interactors nominated that TRIM28 is indispensable for TRIM24 protein stability. We showed that TRIM28 stabilizes TRIM24 against SPOP-mediated ubiquitination and degradation. TRIM28 promotes TRIM24 and AR transcription activity, androgen-dependent and -independent PCa growth. In addition, we demonstrated that TRIM28 level in high in advanced PCa, which drives TRIM24/AR transcription activity in a similar manner to SPOP mutation, which implies that TRIM28 potentially dictates the therapeutic outcome of TRIM24-targeted therapy.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
20 Samples
Download data: TXT
Series
Accession:
GSE108145
ID:
200108145
15.

TRIM28 protects TRIM24 from SPOP-mediated degradation and promotes prostate cancer progression [ChIP-seq]

(Submitter supplied) In this study, proteomic profiling of TRIM24 interactome in conjunction with shRNA screening of TRIM24 top-interactors nominated that TRIM28 is indispensable for TRIM24 protein stability. We showed that TRIM28 stabilizes TRIM24 against SPOP-mediated ubiquitination and degradation. TRIM28 promotes TRIM24 and AR transcription activity, androgen-dependent and -independent PCa growth. In addition, we demonstrated that TRIM28 level in high in advanced PCa, which drives TRIM24/AR transcription activity in a similar manner to SPOP mutation, which implies that TRIM28 potentially dictates the therapeutic outcome of TRIM24-targeted therapy.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL15456
7 Samples
Download data: BEDGRAPH, TXT
Series
Accession:
GSE108144
ID:
200108144
16.

Global transcriptional profiling changes upon knockdown of G9a in human non-small cell lung cancer cells

(Submitter supplied) The experiment was designed to display differential gene expression profiling changes in two human Non-small cell lung cancer cells upon knockdown of G9a/EHMT2, by using RNAseq technology.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
8 Samples
Download data: TXT
17.

H3K9 Trimethylation Silences Fas Expression to Confer Colon Carcinoma Immune Escape and 5-Fluorouracil Chemoresistance

(Submitter supplied) We have determined that verticillin A is a histone methyltransfease inhibitor that selectively inhibits human SUV39H1, SUV39H2, G9a and GLP to inhibit H3K9 methylation in human colon cancer cells. The objective here is to identify verticillin A target genes in human colon cancer cells.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL16686
4 Samples
Download data: CEL
Series
Accession:
GSE51262
ID:
200051262
18.

Expression data from knockdown of G9a in MDA-MB231 cells

(Submitter supplied) G9a is an H3K9m2 methyltransferase, which is critical in controlling gene suppression and DNA methylation. We used microarray analysis to identify the target genes that are regulated by G9a in MDA-MB231 cells, in which E-cadherin is silenced.
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS4800
Platform:
GPL6244
6 Samples
Download data: CEL, CHP
Series
Accession:
GSE34925
ID:
200034925
19.
Full record GDS4800

H3K9me2 methyltransferase G9a depletion effect on breast cancer cell line

Analysis of MDA-MB231 breast cancer cells depleted for G9a, a methyltransferase that mediates histone H3 lysine-9 di-methylation (H3K9me2). G9a depletion inhibits migratory ability and invasiveness of MDA-MB231 cells. Results provide insight into role of G9a and H3K9me2 in breast cancer progression.
Organism:
Homo sapiens
Type:
Expression profiling by array, transformed count, 2 genotype/variation sets
Platform:
GPL6244
Series:
GSE34925
6 Samples
Download data: CEL, CHP
20.

PanCancer pathway anaysis of RH41 Human Alveolar Rhabdomyosarcoma (ARMS) cell line

(Submitter supplied) multiplex gene expression analysis with 770 genes from 13 cancer-associated canonical pathways including: MAPK, STAT, PI3K, RAS, Cell Cycle, Apoptosis, Hedgehog, Wnt, DNA Damage Control, Transcriptional Regulation, Chromatin Modification, and TGF-ẞ.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL19956
4 Samples
Download data: XLSX
Series
Accession:
GSE118777
ID:
200118777
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