LNCaP clone FGC; LNCaP.FGC
Cat.No.: CSC-C9478L
Species: Homo sapiens (Human)
Source: Lymph Node Metastasis
Morphology: epithelial
Culture Properties: adherent, single cells and loosely attached clusters
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- Background
- Scientific Data
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vWA: 16,18
FGA: 19,20
Amelogenin: X,Y
TH01: 9
TPOX: 8,9
CSF1P0: 10,11
D5S818: 11,12
D13S317: 10,12
D7S820: 9,11
LNCaP clone FGC is a human prostate adenocarcinoma cell line, isolated from a metastatic lesion in the left supraclavicular lymph node of a 50-year-old Caucasian guy with advanced prostate cancer. LNCaP clone FGC is a subclone of the parental LNCaP line and maintains many of the molecular and behavioral features that have made it one of the most commonly utilized in vitro models for prostate cancer research.
The cells display an epithelial shape, express functional androgen receptors (AR) and show a very high responsiveness to androgen stimulation. LNCaP clone FGC cells also generate prostate-specific antigen (PSA) and prostate-specific acid phosphatase (PSAP), which are therapeutically important indicators for assessing androgen signaling and prostate cancer progression. These cells represent an essential model of AR-regulated gene expression, hormone-dependent tumor growth and mechanisms of resistance to androgen deprivation therapy due to their androgen-sensitive phenotype.
The LNCaP clone FGC cells have been widely used as a model system to study prostate cancer biology, cancer metabolism, signal transduction, epigenetic regulation, drug discovery and therapeutic development. They are especially useful for testing new anti-androgen drugs and tailored therapy. LNCaP clone FGC cells also provide a gold-standard model for fundamental and translational prostate cancer research due to their defined genetic background and repeatable in vitro and in vivo performance.
Cellular and Molecular Progression of Prostate Cancer: Models for Basic and Preclinical Research
Background
This review discusses the cellular and molecular progression of prostate cancer, from prostate intraepithelial neoplasia to metastatic, castration-resistant disease, highlighting key genetic alterations such as PTEN loss, NKX3.1 loss, MYC activation, TMPRSS2-ERG fusion, and AR mutations. It then surveys in vitro and in vivo research models, including non-cancerous and cancerous prostate cell lines, genetically engineered mouse models, patient-derived xenografts, 3D organoids, rat and zebrafish models. The authors compare advantages and limitations and emphasize the need for models reflecting racial disparities to advance basic and preclinical prostate cancer research.
Key Findings
The review finds that prostate cancer progression is driven by sequential molecular alterations: early loss of PTEN and NKX3.1, MYC overexpression, GSTP1 inactivation, SPOP mutation, and TMPRSS2-ERG fusion characterize PIN; advanced adenocarcinoma involves RB1 loss, telomerase activation, and FOXA1 mutation; metastasis involves SMAD4 loss, AR alterations, CXCL12/CXCR4, RANK-RANKL, EMT, and EZH2. Numerous models are available: non-cancerous lines (RWPE-1, BPH-1, pRNS-1-1, RC-77N/E, HprEpC), castration-sensitive lines (LNCaP, LAPC-4/9, VCaP, MDA-PCa 2a/2b, LuCaP 23.1, RC-77T/E), castration-resistant lines (C4-2/C4-2B, 22Rv1, PC-3, DU-145, ARCaP), GEMMs (TRAMP, LADY, Pten-null, Pten/Smad4, Hi/Lo-Myc, MPAKT), patient-derived xenografts, 3D organoids, rat and zebrafish models. Each model has specific advantages and limitations; cell lines are inexpensive but lack heterogeneity, while PDXs and GEMMs better mimic human disease but are costly and time-consuming. The authors conclude that complementary models and race-specific models are needed.
Contribution
Creative Bioarray is acknowledged in Table 1 as a commercial source of several prostate cell lines, including BPH-1, LNCaP, PC-3, and 22Rv1. Its provision of these validated models supports in vitro prostate cancer research and the review's cataloging of available model systems.
Comprehensive Genomic Landscape of the LNCaP_FGC Prostate Cancer Cell Line
To address the limited availability of representative prostate cancer models, Bose et al. systematically characterized the LNCaP_FGC subline. Whole-genome sequencing (WGS) of LNCaP_FGC (CRL-1740) generated 40× coverage, revealing a highly mutated genome with 409,210 single nucleotide variants (134.46 mutations/Mb) and an estimated tumor ploidy of 3.2, indicative of mixed diploid and tetraploid populations (Fig. 1A). Structural analysis identified widespread alterations, with 27% of the genome affected by copy number changes, including arm-level deletions on chromosomes 2q and 13, and 321 large-scale rearrangements (deletions, duplications, inversions, and translocations).
Genomic analysis confirmed four major oncogenic driver events recurrent in metastatic prostate cancer: (a) the T878A point mutation in the androgen receptor (AR); (b) a complex rearrangement involving the ETS oncogene ETV1; (c) biallelic loss of the PTEN tumor suppressor; and (d) genomic disruption of DNA mismatch repair genes MSH2 and MSH6, correlating with the observed hypermutation (Figs. 1A-E). These data provide a high-resolution molecular blueprint of the LNCaP_FGC model, defining its utility and limitations for preclinical research.
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