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GPRC5A facilitates cell proliferation and bone metastasis of prostate cancer.

ABSTRACT: GPRC5A facilitates cell proliferation and bone metastasis of prostate cancer.

PROVIDER: PRJNA497056 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8062801_1.fastq.gz	Fastqsanger.gz
	SRR8062801_2.fastq.gz	Fastqsanger.gz
	SRR8062802_1.fastq.gz	Fastqsanger.gz
	SRR8062802_2.fastq.gz	Fastqsanger.gz
	SRR8062803_1.fastq.gz	Fastqsanger.gz

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GPRC5A facilitates cell proliferation and bone metastasis of prostate cancer.

Project description:Prostate cancer is a high frequent disease. Early stage prostate cancer can be cured with high probability by early treatment, but hormone refractory prostate cancer and progressive prostate cancer is poor prognosis. Orphan GPCRs have the potential to become a drug discovery target in various carcinomas, but there are few reports in prostate cancer and there are still many possibilities. By big data analysis, we focused on the biological properties of the prostate cancer cell line and found GPRC5A from Orphan GPCR as one of the regulators of prostate cancer development. GPRC5A knock out by genomic editing in PC3, proliferative ability and bone metastasis was markedly suppressed. In prostate cancer cells, GPRC5A inhibit phosphorylation of CREB and affected the expression of cell cycle related genes. GPRC5A is also involved in the establishment of bone metastases, and correlated with prostate cancer metastasis and prognosis. These dates suggest that GPRC5A facilitates cell proliferation and progression of prostate cancer and can be a target for new prognostic marker or drug discovery of prostate cancer.

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Expression data from Gprc5a wild type or knockout mouse tracheal epithelial cells (MTECs)

Project description:Gprc5a is a lung tumor suppressor gene. Gprc5a-knockout (ko) mice can develop spontaneous lung cancer and Gprc5a-ko mouse model is relevant to human lung cancer. Thus, exploration of the mechanisms underlying lung tumorigenesis in Gprc5a-ko mice would be very helpful for revealing those in human lung cancer. We used microarrays to detail the global gene expression profile that underlies oncogenesis by Gprc5a-knockout gene deletion in mouse tracheal epithelial cells. Wild type and gene-knockout mouse tracheal epithelial cells that were divided into two groups were used for RNA extraction.

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Differential gene expression patterns signifying loss of the mouse tumor supressor Gprc5a in lung epithelial cells

Project description:Increasing the understanding of the impact of changes in oncogenes and tumor suppressor genes is essential for improving the management of lung cancer. Recently, we identified a new mouse lung-specific tumor suppressor - the G-protein coupled receptor 5A (Gprc5a). We sought to understand the molecular consequences of Gprc5a loss and towards this we performed microarray analysis of the transcriptomes of lung epithelial cells cultured from normal tracheas of Gprc5a knockout and wild-type mice to define a loss-of-Gprc5a gene signature. Gprc5a wild type cells (WT-NLE) and Gprc5a knockout cells (NULL-NLE) were isolated and cultured from trachea of three week old Gprc5a wild type and knockout mice, respectively. Following RNA extraction and purification, the transcriptome of the Gprc5a wild type and knockout cells were analyzed by microarray analysis using the Affymetrix MG-430 2.0 murine array platform.

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RNA-sequencing of lung tissues from Gprc5a-/- and Gprc5a-/-/Lcn2-/- mice at baseline and seven months post-NNK

Project description:We have shown that Gprc5a-/- mice form Kras-mutant lung tumors spontaneously which is accelerated by tobacco carcinogen (NNK) exposure. We found in these mice that Lcn2 was distinctively up-regulated along the spectrum of Kras-mutant lung cancer development. To understand the role of Lcn2 in lung cancer pathogenesis, we generated Gprc5a-/-/Lcn2-/- mice and found that these animals have increased lung tumor devleopment following NNK compared to Gprc5a-/- animals with intact Lcn2. To understand these effects, we performed RNA-sequencing (RNA-Seq) of lung tissues from Gprc5a-/-/Lcn2-/- and Gprc5a-/- mice at baseline (prior to NNK exposure) and of tumor-bearing lungs from both groups at seven months post-NNK exposure.

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HDAC2 facilitates metastasis of pancreatic cancer cells

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Expression data from Gprc5a wild type or knockout mouse tracheal epithelial cells (MTECs)

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Elevation of GPRC5A expression in colorectal cancer promotes tumor progression through VNN-1 induced oxidative stress

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