ArticlePloS one2014
Comparative genomic and transcriptomic analyses of LNCaP and C4-2B prostate cancer cell lines.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 46 citations in OpenAlex.
- Identifying myosin heavy chain 11 as a predictive biomarker of prostate cancer progression and antiandrogen resistance.Oncology letters · 2026Article
- Extracellular vesicle-mediated delivery of CRISPR machinery silences androgen receptor in castration-resistant prostate cancer cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Bruceine D attenuates prostate cancer growth and motility by suppressing PI3K/AKT signaling and downregulating CXCL16: implications for skeletal metastasis in orthopedic oncology.Frontiers in pharmacology · 2026Article
- Targeting SOX4/PCK2 signaling suppresses neuroendocrine trans-differentiation of castration-resistant prostate cancer.Biology direct · 2024Article
- Hypoxia-inducible factor 1A inhibition overcomes castration resistance of prostate tumors.EMBO molecular medicine · 2023Article
- Hybrid Androgen Receptor Inhibitors Outperform Enzalutamide and EPI-001 in in vitro Models of Prostate Cancer Drug Resistance.ChemMedChem · 2023Article
- Prostate cancer addiction to oxidative stress defines sensitivity to anti-tumor neutrophils.Clinical & experimental metastasis · 2022Article
- Identification of Novel Pyroptosis-Related Gene Signatures to Predict Prostate Cancer Recurrence.Frontiers in oncology · 2022Article
- An integrated functional and clinical genomics approach reveals genes driving aggressive metastatic prostate cancer.Nature communications · 2021Article
- Resistance to Antiandrogens in Prostate Cancer: Is It Inevitable, Intrinsic or Induced?Cancers · 2021Review
- SETD1A Promotes Proliferation of Castration-Resistant Prostate Cancer Cells via FOXM1 Transcription.Cancers · 2020Article
- Role of αVβ3 in Prostate Cancer: Metastasis Initiator and Important Therapeutic Target.OncoTargets and therapy · 2020Review
- Targeted alpha therapy in a systemic mouse model of prostate cancer - a feasibility study.Theranostics · 2020Article
- Paxillin regulated genomic networks in prostate cancer.Steroids · 2019Article
- Molecular determinants of response to high-dose androgen therapy in prostate cancer.JCI insight · 2019Article
- Nerve Growth Factor Induces Proliferation and Aggressiveness In Prostate Cancer Cells.Cancers · 2019Article
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- Whole-Genome Sequence of the Metastatic PC3 and LNCaP Human Prostate Cancer Cell Lines.G3 (Bethesda, Md.) · 2017Article
- Src promotes castration-recurrent prostate cancer through androgen receptor-dependent canonical and non-canonical transcriptional signatures.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The LNCaP and C4-2B cell lines form an excellent preclinical model to study the development of metastatic castration-resistant prostate cancer, since C4-2B cells were derived from a bone metastasis that grew in nude mice after inoculation with the LNCaP-derived, castration-resistant C4-2 cells. Exome sequencing detected 2188 and 3840 mutations in LNCaP and C4-2B cells, respectively, of which 1784 were found in both cell lines. Surprisingly, the parental LNCaP cells have over 400 mutations that were not found in the C4-2B genome. More than half of the mutations found in the exomes were confirmed by analyzing the RNA-seq data, and we observed that the expressed genes are more prone to mutations than non-expressed genes. The transcriptomes also revealed that 457 genes show increased expression and 246 genes show decreased expression in C4-2B compared to LNCaP cells. By combining the list of C4-2B-specific mutations with the list of differentially expressed genes, we detected important changes in the focal adhesion and ECM-receptor interaction pathways. Integration of these pathways converges on the myosin light chain kinase gene (MLCK) which might contribute to the metastatic potential of C4-2B cells. In conclusion, we provide extensive databases for mutated genes and differentially expressed genes in the LNCaP and C4-2B prostate cancer cell lines. These can be useful for other researchers using these cell models.
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