CWR22Rv1-AR-EK cell line

Resistance to androgen receptor (AR)-targeted therapies in prostate cancer (PC) is a major clinical problem. A key mechanism of treatment resistance in advanced PC is the generation of alternatively spliced forms of the AR termed AR variants (AR-Vs) that are refractory to targeted agents and drive tumour progression. Our understanding of how AR-Vs function is limited due to difficulties in distinguishing their discriminate activities from full-length AR (FL-AR)._x000D_ _x000D_ The CWR22Rv1-AR-EK (Androgen Receptor-Exon Knockout) cell line is a prostate cancer cell line which is knockout for FL-AR (by CRISPR) but retains expression of all endogenous AR-Vs making it a valuable…

Contributors

Inventor Institute
Luke Gaughan Newcastle University
Cat. #: 154854
Tool sub type: Continuous
Unit size: 1×10^6 cells / vial
Cancer types: Prostate cancer
Research Fields: Cancer;Drug development
Organism: Human
Model: Knock-In
Cancer Types In Detail: Prostate
Alternate name: AR-V
Product description: Resistance to androgen receptor (AR)-targeted therapies in prostate cancer (PC) is a major clinical problem. A key mechanism of treatment resistance in advanced PC is the generation of alternatively spliced forms of the AR termed AR variants (AR-Vs) that are refractory to targeted agents and drive tumour progression. Our understanding of how AR-Vs function is limited due to difficulties in distinguishing their discriminate activities from full-length AR (FL-AR).The CWR22Rv1-AR-EK (Androgen Receptor-Exon Knockout) cell line is a prostate cancer cell line which is knockout for FL-AR (by CRISPR) but retains expression of all endogenous AR-Vs making it a valuable model for the study of receptor splice variants. This new derivative is dependent upon AR-Vs for growth and is refractory to all FL-AR-targeting agents. CRISPR edited CWR22Rv1 cells.
Conditional: No
Production details: CRISPR-derived cell line that has lost expression of full length androgen receptor (FL-AR), but retains all endogenous androgen receptor variants (AR-Vs). Two gRNAs were designed to target distinct loci within exon 5 of the AR gene. To knock-in a stop codon into exon 5 of the AR locus, a 180 bp ssODN template was designed containing a central TAA sequence and flanked by 75 bp 5â?‚€?‹Â› and 3â?‚€?‹Â› termini 100% complementary to the AR gene sequence.
Additional notes: CRISPR edited CWR22Rv1 cells. Cancer Research Technology Limited (trading research tools as Ximbio) has been granted a non-exclusive license to the CRISPR-Cas9 technology by ERS Genomics Ltd under the patent rights listed here. This license from ERS Genomics Ltd allows Ximbio to develop and commercialise CRISPR-Cas9 modified cell lines for research use only. Ximbio can pr…
Parental cell line: CWR22Rv1
disease: Cancer
Format: Frozen
Storage conditions: Liquid Nitrogen
Shipping conditions: Dry ice
Growth medium: RPMI 1640 media supplemented with 10% foetal calf serum (FCS) and 5% L-glutamine at 37?‚°C
Recommended controls: CWR22Rv1 parental line
Mycoplasma free: Yes
Biosafety level: 1
References:

Kounatidou et al. 2019. Nucleic Acids Res. 47(11):5634-5647. PMID: 31006810.

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