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.
Choline Kinase Alpha as an Androgen Receptor Chaperone and Prostate Cancer Therapeutic Target.
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Nuclear ARRB1 induces pseudohypoxia and cellular metabolism reprogramming in prostate cancer.
Specimen part, Cell line
View SamplesBeta-arrestin 1 (ARRB1) has been implicated in transcriptional regulation as part of protein complexes bound to chromatin. Here we investigate its effect on transcription and its potential impact on prostate cancer. We report the first genome-wide mapping of chromatin binding for ARRB1 and combine it with expression array data to define its transcriptome. We identify Hypoxia Inducible Factor 1A (HIF1A) as a nuclear binding partner that recruits ARRB1 to promoter regions of HIF1A targets. We show that ARRB1 modulates HIF1A-dependent transcription and promotes a shift in cellular metabolism from oxidative phosphorylation to aerobic glycolysis. In addition, we show that ARRB1 plays an important role in neoplastic transformation, cell growth and resistance to hypoxic stress. This is the first example of an endocytic adaptor protein regulating metabolic pathways and implicates ARRB1 as a tumour promoter.
Nuclear ARRB1 induces pseudohypoxia and cellular metabolism reprogramming in prostate cancer.
Specimen part, Cell line
View SamplesComparison of the transcriptome of human kideny cancer cells either wild-type for FH or FH-deficient. The UOK262 cells were isolated from mediastinum metastasis of a HLRCC patient (Yang et al. Cancer Genetics and Cytogenetics, Volume 196, Issue 1, 1 January 2010, Pages 45–55). FH function was restored in the UOK262 by re-expressing the FH transcript from an exogenous plasmid. Overall design: Examination of gene transciption in 2 cell types.
Fumarate is an epigenetic modifier that elicits epithelial-to-mesenchymal transition.
No sample metadata fields
View SamplesComparison of the transcriptome of immortalised mouse kidney epithelial cells either wt for Fh1 or Fh1-deficient. The cells were isolated from kidneys of P5 mouse(see Frezza et al, Nature 2011). Briefly, Fh1_fl (flox) are wt for Fh1 (floxed cassette not excised), clone 1 and clone 19 are two different Fh1-deificent clones (floxed cassette excised) and Rec are clone 19 with reconstituted Fh1 expression from exogenous plasmid. Overall design: Examination of gene transciption in 4 cell types.
Fumarate is an epigenetic modifier that elicits epithelial-to-mesenchymal transition.
Specimen part, Cell line, Subject
View SamplesDetailed analysis of androgen regulated gene expression in the LNCaP prostate cancer cell line. Since androgens and the AR are known to be important for prostate cancer cell proliferation and invasion we aimed to identify androgen receptor (AR) regulated genes by combining this detailed Illumina beadarray study of androgen regulated gene expression with AR ChIP-sequencing data.
The androgen receptor fuels prostate cancer by regulating central metabolism and biosynthesis.
Specimen part, Time
View SamplesAnalysis 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.
A reciprocal feedback between the PDZ binding kinase and androgen receptor drives prostate cancer.
No sample metadata fields
View SamplesAnalysis 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.
A reciprocal feedback between the PDZ binding kinase and androgen receptor drives prostate cancer.
No sample metadata fields
View SamplesUsing a chromatin regulator-focused shRNA library, we found that suppression of sex determining region Y-box 10 (SOX10) in melanoma causes resistance to BRAF and MEK inhibitors. To investigate how SOX10 loss leads to drug resistance, we performed transcriptome sequencing (RNAseq) of both parental A375 (Ctrl. PLKO) and A375-SOX10KD (shSOX10-1, shSOX10-2) cells. To ask directly whether SOX10 is involved indrug resistance in BRAF(V600E) melanoma patients, we isolated RNA from paired biopsies from melanoma patients (pre- and post- treatment) , that had gained BRAF or MEK inhibitor resistance . We performed RNAseq analysis to determine changes in transcriptome upon drug resistance. Overall design: Investigate genes regulated by SOX10 and differntial gene expression between pre- and post-treatment biopsies. We use short hairpin RNA to suppression SOX10 in A375 cells and cells were harvested with trizol reagent for RNA isolation. For paired biopsies (patient samples) we collected the first biopsy before the initiation of treatment and the second biopsy after drug resistance developed. RNA was isolated from FFPE samples and subjected for RNA sequencing.
Reversible and adaptive resistance to BRAF(V600E) inhibition in melanoma.
Sex, Age, Specimen part, Cell line, Subject
View SamplesIdentification of relevant subgroups in childhood MDS patients by gene expression analysis and gene involve in progression into AML
Gene expression signatures of pediatric myelodysplastic syndromes are associated with risk of evolution into acute myeloid leukemia.
Specimen part, Disease
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