Androgen Receptor splice variant V7 (AR-V7) mediates AR signalling in castration resistant prostate cancer (CRPC) [RNA-seq]
Source: NCBI BioProject (ID PRJNA602080)
Source: NCBI BioProject (ID PRJNA602080)
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Project name: Androgen Receptor splice variant V7 (AR-V7) mediates AR signalling in castration resistant prostate cancer (CRPC) [RNA-seq]
Description: CRPC remains AR dependent. There are multiple mechanisms for reactivation of AR including expression of constitutively active AR splices variant AR-V7 (AR3). Earlier studies suggest that though the variants regulate many of the same genes as AR, they also have unique targets. Another argument is that the variant is a “weak” AR. We have used an LNCaP cell line that expresses AR-V7 in response to doxycycline (LNCaP AR-V7) to compare the activities of the two isoforms and to identify differential regulation of target genes. We also used VCaP cell line that expresses AR-V7 in response to doxycycline (VCaP AR-V7) to validate the activities of the two isoforms in an alternative prostate cancer cell line. The transcriptomes for AR and AR-V7 in these cell lines were identified using RNA-Seq.Overall design: Biological replicates of LNCaP AR-V7 and VCaP AR-V7 cells treated with ethanol, 10uM R1881 or 20ng/mL Doxycycline for 24 hours were harvested into PureXtract RNAzol solution. Total RNA was extracted, and column purified using RNAeasy kit (Qiagen, USA). Equal amounts of clean total RNA samples from biological replicates were pooled together for library preparation.
Data type: Transcriptome or Gene expression
Sample scope: Multiisolate
Relevance: Medical
Organization: MD Anderson Cancer Center
Literatures
- PMID: 35354884
Last updated: 2020-01-18