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Homo sapiens

ABSTRACT: RNA-seq analysis of BAP18 knockdown in prostate cancer cell line 22Rv1

PROVIDER: PRJNA320835 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3479286_1.fastq.gz	Fastqsanger.gz
	SRR3479286_2.fastq.gz	Fastqsanger.gz
	SRR3480701_1.fastq.gz	Fastqsanger.gz
	SRR3480701_2.fastq.gz	Fastqsanger.gz
	SRR3480702_1.fastq.gz	Fastqsanger.gz

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Project description:RNA-Seq of prostate cancer cell line 22RV1

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Multi omics analysis of adaptation to repeated DNA damage in prostate cancer cells.

Project description:DNA damage is frequently utilized as the basis for cancer therapies; however, resistance to DNA damage remains one of the biggest challenges facing cancer patients and their treating clinicians. Critically, the molecular drivers behind resistance are poorly understood. To address this question, we created an isogenic model of prostate cancer exhibiting more aggressive characteristics to better understand the molecular signatures associated with resistance and metastasis. 22Rv1 cells were repeatedly exposed to DNA damage daily for 6 weeks, similar to patient treatment regimes. Using Illumina MethylationEPIC arrays and RNA-seq, we compared the DNA methylation and transcriptional profiles between the parental 22Rv1 cell line and the lineage exposed to prolonged DNA damage. Here we show that repeated DNA damage drives the molecular evolution of cancer cells to a more aggressive phenotype and identify molecular candidates behind this process. Total DNA methylation was increased in cells exposed to repeated DNA damage. Further, RNA-seq demonstrated these cells had dysregulated expression of genes involved in metabolism and the unfolded protein response (UPR) with ASNS identified as central to this process. While limited overlap between RNA-seq and DNA methylation was evident, OGDHL was identified as altered in both data sets. Utilising a second approach we profiled the proteome in 22Rv1 cells following a single dose of radiotherapy. This analysis also highlighted the UPR in response to DNA damage. Together, these analyses identified dysregulation of metabolism and the UPR and identified ASNS and OGDHL as candidate genes for resistance to DNA damage. This work provides critical insight into molecular changes which may underpin treatment resistance and metastasis.

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Project description:To investigate the function of ZMYND11 in prostate cancer, we knockdown ZMYND11 in 22Rv1 cells and do RNA-seq.

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Prostate cancer cell lines: non-targeting siRNA versus SChLAP1-siRNA treated

Project description:SChLAP1 is a novel long non-coding RNA expressed in prostate cancer. Here we performed transcriptional profiling of the prostate cancer cell lines LNCaP and 22Rv1 comparing non-targeting siRNA treatment versus SChLAP1-siRNA treatment. Goal was to determine the effect of SChLAP1 knockdown on gene expression in prostate cancer. Two-condition experiment: non-targeting siRNA versus SChLAP1 siRNA treated cells. Biological replicates: 1 control replicate, 2 treatment replicates. Technical replicates: 3 replicates per SChLAP1 siRNA. Cell lines: 22Rv1 and LNCaP.

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