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accession-icon GSE55322
Validated prediction of pro-invasive growth factors using a transcriptome-wide invasion signature derived from a complex 3-D invasion assay
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The invasion of activated fibroblasts represents a key pathomechanism in fibrotic diseases, carcinogenesis and metastasis. Here, invading fibroblasts contribute to fibrotic extracellular matrix (ECM) formation and the initiation, progression, or resistance of cancer, respectively. To construct a transcriptome-wide signature of fibroblast invasion, we used a multiplex phenotypic 3D invasion assay using murine lung fibroblasts. Microarray-based gene expression profiles of invading and non-invading fibroblasts were highly distinct: 1049 genes were differentially regulated (>1.5-fold). An unbiased pathway analysis (Ingenuity) identified a significant enrichment for the functional clusters invasion of cells, idiopathic pulmonary fibrosis (IPF) and metastasis. Particularly, matrix metalloprotease13 (MMP13), transforming growth factor (TGF)1, Caveolin1 (Cav1), Phosphatase and Tensin Homolog (Pten), and secreted frizzled-related protein1 (Sfrp1) were among the highest regulated genes. In silico analysis by Ingenuity predicted TGF1, epidermal growth factor (EGF), fibroblast growth factor2 (FGF2), and platelet-derived growth factor (PDGF)-BB to induce invasion. As such, these growth factors were tested in the 3D invasion assay and displayed a significant induction of invasion, thus validating the transcriptome profile. Accordingly, our transcriptomic invasion signature describes the invading fibroblast phenotype in unprecedented detail and provides a tool for future functional studies of cell invasion and therapeutic modulation thereof.

Publication Title

Validated prediction of pro-invasive growth factors using a transcriptome-wide invasion signature derived from a complex 3D invasion assay.

Sample Metadata Fields

Sex

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accession-icon SRP184695
A novel CRISPR-engineered prostate cancer cell line defines the AR-V transcriptome and identifies PARP inhibitor sensitivities.
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Development of a novel CRISPR-derived cell line which is a derivative of CWR22Rv1 cells, called CWR22Rv1-AR-EK, that has lost expression of FL-AR, but retains all endogenous AR-Vs. AR-Vs act unhindered by loss of FL-AR to drive cell growth and expression of androgenic genes. Global transcriptomics demonstrate that AR-Vs drive expression of a cohort of DNA damage response genes and depletion of AR-Vs sensitizes cells to ionizing radiation. Overall design: Transcriptomic profile (mRNA) of AR splice variants in CWR22Rv1 AR-EK cells was generated by deep sequencing, in triplicate, using Illumina HiSeq 2500.

Publication Title

A novel CRISPR-engineered prostate cancer cell line defines the AR-V transcriptome and identifies PARP inhibitor sensitivities.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE65738
Effect of over-expression of AR-V7 in MDA-MB-453 breast cancer cells
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

The effect of transient transfection of a construct designed to over-express the androgen receptor (AR) variant AR-V7 on gene expression in MDA-MB-453 cells was assessed using Affymetrix Gene 2.0 ST arrays. Transfection of an AR-expressing construct or an empty construct served as controls.

Publication Title

Expression of androgen receptor splice variants in clinical breast cancers.

Sample Metadata Fields

Cell line

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accession-icon SRP051333
Effect of PDZ domain binding Kinase inhibition using TOPK-32 (called PBKi) on C4-2 cell transcriptome
  • organism-icon Homo sapiens
  • sample-icon 48 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Analysis of C4-2 prostate cancer cell line after 6 hrs of treatment with TOPK-32. PBK is overexpressed in a number of solid tumours, including prostate cancer. Results provide insight into the molecular mechanisms of PBK in prostate carcinogenesis. Overall design: This experiment was designed to understand the regulation of transcriptome by PDZ domain binding kinase, which is an important kinase with role in cell cycle. The cells were treated with a catalytic inhibitor TOPK32 which inhibits the kinase activity of PBK protein.

Publication Title

A reciprocal feedback between the PDZ binding kinase and androgen receptor drives prostate cancer.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP050332
Effect of PBK knockdown on C4-2 cell transcriptome
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Analysis of C4-2 Prostate cancer cell line after 72 hours of knockdown. PBK is overexpressed in a number of solid tumours, including prostate cancer. Results provide insight into the molecular mechanisms of PBK in prostate carcinogenesis. Overall design: This experiment was designed to understand the regulation of transcriptiome by PDZ domain binding kinase (PBK), which is an important kinase with role in cell cycle. In order to achieve this, the endogenous protein was knocked down using siRNA pool that targets the PBK mRNA.

Publication Title

A reciprocal feedback between the PDZ binding kinase and androgen receptor drives prostate cancer.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP144499
Gene expression analysis of prostate cancer cells treated with fatty acid synthase (FASN) inhibitor IPI-9119
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Alterations in gene expression following fatty acid synthase inhibtion were evaluated in androgen sensitive LNCaP cells and castration resistant 22Rv1 and LNCaP-95 cells. Cell were exposed to 2 concentrations (0.1 and 0.5 uM) of FASN inhibitor IPI-9119 or DMSO for 6 days. Overall design: Differential gene expression anlaysis in 3 prostate cancer cell lines treated with FASN inhibitor IPI-9119

Publication Title

Inhibition of de novo lipogenesis targets androgen receptor signaling in castration-resistant prostate cancer.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP050331
Effect of CHKA knockdown on C4-2 cell transcriptome
  • organism-icon Homo sapiens
  • sample-icon 48 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Analysis of C4-2 Prostate cancer cell line after 72 hours of knockdown. CHKA is overexpressed in a number of solid tumours, including prostate cancer. Results provide insight into the molecular mechanisms of CHKA in prostate carcinogenesis. Overall design: This experiment was designed to understand the regulation of transcriptome by Choline kinase alpha (CHKA) which is an important enzyme in Kennedy pathway. In order to achieve this, the endogenous protein was knocked down using siRNA pool that targets the CHKA mRNA.

Publication Title

Choline Kinase Alpha as an Androgen Receptor Chaperone and Prostate Cancer Therapeutic Target.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE16464
Chondrogenic differentiation potential of OA chondrocytes and their use in autologous chondrocyte transplantation
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Autologous chondrocyte transplantation (ACT) is a routine technique to regenerate focal cartilage lesions. However, patients with osteoarthritis (OA) are lacking an appropriate long-lasting treatment alternative, partly since it is not known if chondrocytes from OA patients have the same chondrogenic differentiation potential as chondrocytes from donors not affected by OA. Articular chondrocytes from patients with OA undergoing total knee replacement (Mankin Score >3, Ahlbck Score >2) and from patients undergoing ACT, here referred to as normal donors (ND), were isolated applying protocols used for ACT. Their chondrogenic differentiation potential was evaluated both in high-density pellet and scaffold (Hyaff-11) cultures by histological proteoglycan assessment (Bern Score) and immunohistochemistry for collagen types I and II. Chondrocytes cultured in monolayer and scaffolds were subjected to gene expression profiling using genome-wide oligonucleotide microarrays. Expression data were verified by using quantitative RT-PCR. Chondrocytes from ND and OA donors demonstrated accumulation of comparable amounts of cartilage matrix components, including sulphated proteoglycans and collagen types I and II. The mRNA expression of cartilage markers (COL2A1, COMP, aggrecan, CRTL1, SOX9) and genes involved in matrix synthesis (biglycan, COL9A2, COL11A1, TIMP4, CILP2) was highly induced in 3D cultures of chondrocytes from both donor groups. Genes associated with hypertrophic or OA cartilage (COL10A1, RUNX2, periostin, ALP, PTHR1, MMP13, COL1A1, COL3A1) were not significantly regulated between the two groups of donors. The expression of 661 genes, including COMP, FN1, and SOX9, were differentially regulated between OA and ND chondrocytes cultured in monolayer. During scaffold culture, the differences diminished between the OA and ND chondrocytes, and only 184 genes were differentially regulated. Only few genes were differentially expressed between OA and ND chondrocytes in Hyaff-11 culture. The risk of differentiation into hypertrophic cartilage does not seem to be increased for OA chondrocytes. Our findings suggest that the chondrogenic capacity is not significantly affected by OA and OA chondrocytes fulfill the requirements for matrix-associated ACT.

Publication Title

Chondrogenic differentiation potential of osteoarthritic chondrocytes and their possible use in matrix-associated autologous chondrocyte transplantation.

Sample Metadata Fields

Specimen part

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accession-icon GSE16732
Affymetrix Gene Chip Human Exon 1.0 ST Array expression profiling of 41 human breast cancer cell lines
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)

Description

Gene expression analysis under normal culture conditions (RPMI-10%FBS) and at optimal cell densities.

Publication Title

Low-risk susceptibility alleles in 40 human breast cancer cell lines.

Sample Metadata Fields

Cell line

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accession-icon GSE56989
Genome-wide identification of HIF-1 and HIF-2 binding sites in hypoxic human macrophages alternatively activated by IL-10
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Primary human macrophages with a HIF-1alpha or HIF-2alpha knockdown were pretreated with IL-10 for 16h and afterwards for 4h additionaly under hypoxi (1% O2), RNA was isolated usind the Qiagen RNAeasy Kit and cDNA synthesis wos done using Ambion WT Expression Kit. Expression was compared to si control under control conditions.

Publication Title

Genome-wide identification of hypoxia-inducible factor-1 and -2 binding sites in hypoxic human macrophages alternatively activated by IL-10.

Sample Metadata Fields

Specimen part

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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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Developed by the Childhood Cancer Data Lab

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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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