LNCaP: ARF876L cell line

LNCaP cells are androgen-sensitive human prostate adenocarcinoma cells derived from the left supraclavicular lymph node metastasis from a 50-year-old Caucasian male in 1977. The androgen receptor (AR) in LNCaP cells harbours a T877A mutations which enables the anti-androgen flutamide to act as an agonist.

Contributors

Institute
Northern Institute For Cancer Research, Newcastle University
Cat. #: 154163
Tool sub type: Continuous
Unit size: 1×10^6 cells / vial
Cancer types: Genitourinary cancer
Research Fields: Cancer
Organism: Human
Model: Tumour line
Cancer Types In Detail: Human prostate adenocarcinoma
Alternate name: AR, Dihydrotestosterone Receptor, Nuclear Receptor Subfamily 3 Group C Member 4, NR3C4, DHTR; LNCaP-ARF877L
Product description: LNCaP cells are androgen-sensitive human prostate adenocarcinoma cells derived from the left supraclavicular lymph node metastasis from a 50-year-old Caucasian male in 1977. The androgen receptor (AR) in LNCaP cells harbours a T877A mutations which enables the anti-androgen flutamide to act as an agonist. This cell line is the most commonly used for prostate cancer research. In approximately 30% CRPC, AR mutations are detected and are likely selected for under pressure by hormonal therapies.Mutations within the AR ligand-binding domain, the site of testosterone and anti-androgen binding, enable retention of AR signalling in the presence of hormonal therapies. Two AR LBD mutations are commonly detected in patients treated with bicalutamide and enzalutamide, W741L and F876L,respectively. These convert the activity of anti-androgens from antagonists to agonists and enable progression of CRPC. Modelling these mutations previously has been difficult and have been limited to, principally, luciferase-based assays in non-AR-expressing cell lines. We have therefore developed two key LNCaP cell derivatives that have stable expression of ARW741L (Cat No:154165) and ARF876L mutations which enables us to assess the activity of these aberrantly functioning receptors in a physiological background. Moreover, by depleting endogenous AR in LNCaP cells, we can provide a clean read-out for mutant AR activity that can be utilised for assessing efficacy of novel AR-targeting agents.
Conditional: No
Production details: HEK 293T cells were transfected with pLenti-FLAG-ARF876L to generate viral particles. Using a multiplicity of infection of 0.3 and 0.1, LNCaP cells were transduced with virus. Stable expressing clones were selected with 10Â?„?žg/ml blasticidin. Ectopic AR expression was determined by western blot.
Parental cell line: LNCaP
disease: Cancer
Format: Frozen
Shipping conditions: Dry ice
Growth medium: RPMI-1640 + 10% FBS

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