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accession-icon SRP157582
The Estrogen Receptor variants ß2 and ß5 Induce Stem Cell Characteristics and Chemotherapy Resistance in Prostate Cancer through activation of Hypoxic Signaling
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Chemotherapy resistant prostate cancer is a major clinical problem. When the prostate cancer has become androgen deprivation resistant, one of the few treatment regimens left is chemotherapy. There is a strong connection between a cancer's stem cell like characteristics and drug resistance. By performing RNA-seq we observed several factors associated with stem cells being strongly up-regulated by the estrogen receptor ß variants, ß2 and ß5. In addition, most of these factors were also up-regulated by hypoxia. One mechanism of chemotherapy resistance was expression of the hypoxia-regulated, drug transporter genes, where especially ABCG2 and MDR1 were shown to be expressed in recurrent prostate cancer and to cause chemotherapy resistance by efficiently transporting drugs like docetaxel out of the cells. Another mechanism was expression of the hypoxia-regulated notch3 gene, which causes chemotherapy resistance in urothelial carcinoma, although the mechanism is unknown. It is well known that hypoxic signaling is involved in increasing chemotherapy resistance. Regulation of the hypoxic factors, HIF-1a and HIF-2a is very complex and extends far beyond hypoxia itself. We have recently shown that two of the estrogen receptor ß variants, estrogen receptor ß2 and ß5, bind to and stabilize both HIF-1a and HIF-2a proteins leading to expression of HIF target genes. This study suggests that increased expression of the estrogen receptor ß variants, ß2 and ß5, could be involved in development of a cancer's stem cell characteristics and chemotherapy resistance, indicating that targeting these factors could prevent or reverse chemotherapy resistance and cancer stem cell expansion. Overall design: Examination of the transcriptome changed by two estrogen reseptor beta variants (ERbeta2 and ERbeta5). Control (lacking expression) and variant expressing cells in two repeats

Publication Title

The estrogen receptor variants β2 and β5 induce stem cell characteristics and chemotherapy resistance in prostate cancer through activation of hypoxic signaling.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE33054
Modeling lethal prostate cancer variant with small cell carcinoma features
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Modeling a lethal prostate cancer variant with small-cell carcinoma features.

Sample Metadata Fields

Specimen part, Disease

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accession-icon GSE32967
Modeling lethal prostate cancer variant with small cell carcinoma features [expression profile]
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Purpose: Small-cell prostate carcinoma (SCPC) morphology predicts for a distinct clinical behavior, resistance to androgen ablation, and frequent but short responses to chemotherapy. The model systems we report reflect the biology of the human disease and can be used to improve our understanding of SCPC and to develop new therapeutic strategies for it.

Publication Title

Modeling a lethal prostate cancer variant with small-cell carcinoma features.

Sample Metadata Fields

Specimen part

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accession-icon GSE47050
Expression data from S. cerevisiae following tRNA gene deletion
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

We created a comprehensive tRNA deletion library in yeast and characterized the phenotypic and further characterized the molecular changes in a subset of deletion strains

Publication Title

A comprehensive tRNA deletion library unravels the genetic architecture of the tRNA pool.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE84970
Microarray of CHD1 Knockdown in PC3 cells and CHD1 knockout in LNCaP cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We used microarrays to study the global gene expression and identified differentially expressed genes in CHD1 knockdown PC-3 cells and CHD1 KO LNCaP cells, aiming to identify genes and pathways that are regulated by CHD1

Publication Title

Synthetic essentiality of chromatin remodelling factor CHD1 in PTEN-deficient cancer.

Sample Metadata Fields

Cell line

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accession-icon GSE49287
AR and c-Myb depletion effects in prostate cancer cells
  • organism-icon Homo sapiens
  • sample-icon 60 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Targeting poly(ADP-ribose) polymerase and the c-Myb-regulated DNA damage response pathway in castration-resistant prostate cancer.

Sample Metadata Fields

Cell line

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accession-icon GSE49285
Genome-wide analysis of AR-responsive gene expression in prostate cancer cells
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Analysis of AR-regulation of gene expression. The hypothesis tested in the present study was that AR influences the expression of genes that participate in important bioprocesses in prostate cancer cells, including cell cycle, DNA replication, recombination and repair. Results provide important information on AR-responsive genes that may be crucial to the cell survival and the progression of prostate cancer.

Publication Title

Targeting poly(ADP-ribose) polymerase and the c-Myb-regulated DNA damage response pathway in castration-resistant prostate cancer.

Sample Metadata Fields

Cell line

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accession-icon GSE49286
Genome-wide analysis of c-Myb-responsive gene expression in prostate cancer cells
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Analysis of c-Myb-regulation of gene expression. The hypothesis tested in the present study was that c-Myb influences the expression of specific sets of genes that are involved in cell cycle, DNA replication, recombination and repair. Results provide important information on c-Myb-responsive genes that may be crucial to the cell survival and the progression of prostate cancer.

Publication Title

Targeting poly(ADP-ribose) polymerase and the c-Myb-regulated DNA damage response pathway in castration-resistant prostate cancer.

Sample Metadata Fields

Cell line

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accession-icon GSE46988
Expression data from rat spinal cord injury and mesenchymal stromal cells (MSC) or olfactory ensheathing cells (OEC) transplantation
  • organism-icon Rattus norvegicus
  • sample-icon 52 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.1 ST Array (ragene11st)

Description

We analyzed the changes in the spinal cord transcriptome after a spinal cord contusion injury and MSC or OEC transplantation. The cells were injected immediately or 7 days after the injury. The mRNA of the spinal cord injured segment was extracted and analyzed by microarray at 2 and 7 days after cell grafting.

Publication Title

Gene expression changes in the injured spinal cord following transplantation of mesenchymal stem cells or olfactory ensheathing cells.

Sample Metadata Fields

Treatment

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accession-icon GSE14416
ICSBP-mediated immune protection against BCR-ABL-induced leukemia requires the CCL6 and CCL9 chemokines
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Interferon is effective at inducing complete remissions in patients with Chronic Myelogenous Leukemia (CML), and evidence supports an immune mechanism. Here we show that the Type I Interferons (alpha and beta) regulate expression of the Interferon consensus sequence binding protein (ICSBP) in bcr-abl transformed cells and as shown previously for ICSBP, induce a vaccine-like immunoprotective effect in a murine model of bcr-abl induced leukemia. We identify the chemokines CCL6 and CCL9 as genes prominently induced by the Type I Interferons and ICSBP, and demonstrate that these immunomodulators are required for the immunoprotective effect of ICSBP expression. Insights into the role of these chemokines in the anti-leukemic response of interferons suggest new strategies for immunotherapy of CML.

Publication Title

ICSBP-mediated immune protection against BCR-ABL-induced leukemia requires the CCL6 and CCL9 chemokines.

Sample Metadata Fields

No sample metadata fields

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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