ArticleInternational journal of molecular medicine2017
Androgen-independent LNCaP cells are a subline of LNCaP cells with a more aggressive phenotype and androgen suppresses their growth by inducing cell cycle arrest at the G1 phase.
Article in International journal of molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 40 citations in OpenAlex.
- In vitro cytotoxicity of medicinal plants used in prostate cancer management in Africa: a systematic review.Tropical medicine and health · 2026Review
- WTAP-mediated mScience China. Life sciences · 2025Article
- PSA Secretion from Single Circulating Tumor Cells of Metastatic Castration-Naïve Prostate Cancer Patients.Cancer research communications · 2025Article
- ARv7 promotes the escape of prostate cancer cells from androgen deprivation therapy-induced senescence by mediating the SKP2/p27 axis.BMC biology · 2025Article
- Secretome Analysis of Prostate Cancer Cell Lines Reveals Cell Cycle-Dependent PSA Secretion and Potential Biomarkers.Cancers · 2025Article
- JARID1D-dependent androgen receptor and JunD signaling activation of osteoclast differentiation inhibits prostate cancer bone metastasis through demethylating H3K4.Theranostics · 2025Article
- Co-modulation of a circular form of PCDH11Y during neuroendocrine differentiation of prostate cancer.Frontiers in oncology · 2025Article
- Article
- Exploiting gender-based biomarkers and drug targets: advancing personalized therapeutic strategies in hepatocellular carcinoma.Frontiers in pharmacology · 2024Review
- Targeting Prostate Cancer, the 'Tousled Way'.International journal of molecular sciences · 2023Review
- Loading of "cocktail siRNAs" into extracellular vesicles via TAT-DRBD peptide for the treatment of castration-resistant prostate cancer.Cancer biology & therapy · 2022Article
- Hypoxic Signaling Is Modulated by Calcium Channel, CaV1.3, in Androgen-Resistant Prostate Cancer.Bioelectricity · 2022Article
- Clinical response in metastatic castration-resistant prostate cancer (mCRPC) cases treated with supra-physiological doses of testosterone: Bipolar androgen therapy.Clinical case reports · 2022Article
- PDZRN4 suppresses tumorigenesis and androgen therapy-resistance in prostate cancer.Journal of Cancer · 2022Article
- Identification and Validation of Three Hub Genes Involved in Cell Proliferation and Prognosis of Castration-Resistant Prostate Cancer.Oxidative medicine and cellular longevity · 2022Article
- Osteoblasts Generate Testosterone From DHEA and Activate Androgen Signaling in Prostate Cancer Cells.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2021Article
- The MYH9 Cytoskeletal Protein Is a Novel Corepressor of Androgen Receptors.Frontiers in oncology · 2021Article
- Prostatic aspirated cellular RNA analysis enables fast diagnosis and staging of prostate cancer.Translational oncology · 2021Article
- The metabolic role of PFKFB4 in androgen-independent growth in vitro and PFKFB4 expression in human prostate cancer tissue.BMC urology · 2020Article
- Could the kinetin riboside be used to inhibit human prostate cell epithelial-mesenchymal transition?Medical oncology (Northwood, London, England) · 2020Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Androgen deprivation therapy (ADT, surgical or chemical castration) is the mainstay treatment for metastatic prostate cancer (PCa); however, patients ineluctably relapse despite extremely low androgen levels. This evolution of PCa indicates its lethal progression. In this study, to mimic the traits of clinical PCa progression in vitro, we investigated the alterations in the cell biological characteristics in androgen-independent LNCaP cells (LNCaP-AI cells) compared with LNCaP cells. We also examined the effects of androgen on LNCaP and LNCaP-AI cell proliferation, androgen receptor (AR) expression and prostate-specific antigen (PSA) secretion. Furthermore, AR was silenced in the LNCaP and LNCaP-AI cells to detect the roles taht AR plays in cell growth, apoptosis and PSA secretion. We found that prolonged androgen ablation increased the LNCaP-AI cell growth rate and cell invasiveness, and induced epithelial-mesenchymal transition in the LNCaP-AI cells. Moreover, despite the fact that the LNCaP and LNCaP-AI cells expressed equal amounts of AR protein, androgen induced a greater secretion of PSA in the LNCaP-AI cells than in the LNCaP cells. The proliferation of the LNCaP-AI cells was not dependent on, but was suppressed by androgen, which led to arrest at the G1 phase. Conversely, androgen significantly increased LNCaP cell proliferation by promoting the G1-S transition. Moreover, the silencing of AR suppressed LNCaP and LNCaP-AI cell growth by inducing cell cycle arrest at the G1 phase rather than promoting apoptosis, and reduced PSA secretion. On the whole, our data suggest that LNCaP-AI cells have a more more aggressive phenotype compared with the LNCaP cells; AR remains a critical factor in the LNCaP-AI cells, and androgen suppresses LNCaP-AI cell growth by blocking the cell cycle at the G1 phase.
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