ArticleOncotarget2017
Reversion of epithelial-mesenchymal transition by a novel agent DZ-50 via IGF binding protein-3 in prostate cancer cells.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
- Effect of TGF-β mediated phenotypic changes on prostate cancer cell anoikis response.Oncogene · 2025Article
- Anoikis resistance in Cancer: Mechanisms, therapeutic strategies, potential targets, and models for enhanced understanding.Cancer letters · 2025Review
- Anoikis in phenotypic reprogramming of the prostate tumor microenvironment.Frontiers in endocrinology · 2023Review
- Article
- Role of α- and β-adrenergic signaling in phenotypic targeting: significance in benign and malignant urologic disease.Cell communication and signaling : CCS · 2021Review
- Non-Coding RNAs Set a New Phenotypic Frontier in Prostate Cancer Metastasis and Resistance.International journal of molecular sciences · 2021Review
- Downregulation of LOX promotes castration-resistant prostate cancer progression via IGFBP3.Journal of Cancer · 2021Article
- Review
- Epithelial to Mesenchymal Transition: A Mechanism that Fuels Cancer Radio/Chemoresistance.Cells · 2020Review
- Integrated Therapeutic Targeting of the Prostate Tumor Microenvironment.Advances in experimental medicine and biology · 2020Article
- Restoring E-cadherin Expression by Natural Compounds for Anticancer Therapies in Genital and Urinary Cancers.Molecular therapy oncolytics · 2019Review
- Predictive value of phenotypic signatures of bladder cancer response to cisplatin-based neoadjuvant chemotherapy.Urologic oncology · 2019Article
- [Nucleus translocation of membrane/cytoplasm proteins in tumor cells].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2019Article
- Network-based integrated analysis of omics data reveal novel players of TGF-β1-induced EMT in human peritoneal mesothelial cells.Scientific reports · 2019Article
- Impact of α-adrenoceptor antagonists on prostate cancer development, progression and prevention.American journal of clinical and experimental urology · 2019Review
- Predictive and targeting value of IGFBP-3 in therapeutically resistant prostate cancer.American journal of clinical and experimental urology · 2019Article
- p53-Mediated PI3K/AKT/mTOR Pathway Played a Role in PtoxOxidative medicine and cellular longevity · 2019Article
- GRP78 modulates cell adhesion markers in prostate Cancer and multiple myeloma cell lines.BMC cancer · 2018Article
- Profiling Prostate Cancer Therapeutic Resistance.International journal of molecular sciences · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulation of transforming growth factor-β1 (TGF-β1) and insulin-like growth factor (IGF) axis has been linked to reactive stroma dynamics in prostate cancer progression. IGF binding protein-3 (IGFBP3) induction is initiated by stroma remodeling and could represent a potential therapeutic target for prostate cancer. In previous studies a lead quinazoline-based Doxazosin® derivative, DZ-50, impaired prostate tumor growth by targeting proteins involved in focal adhesion, anoikis resistance and epithelial-mesenchymal-transition (EMT). This study demonstrates that DZ-50 increased expression of the epithelial marker E-cadherin, and decreased the mesenchymal marker N-cadherin in human prostate cancer cells. In DU-145 cells, the effect of DZ-50 on EMT towards mesenchymal epithelial transition (MET) was inhibited by talin1 overexpression, a focal adhesion regulator promoting anoikis resistance and tumor invasion. DZ-50 treatment of human prostate cancer cells and cancer-associated fibroblasts (CAFs) downregulated IGFBP3 expression at mRNA and protein level. In TGF-β1 responsive LNCaPTβRII, TGF-β1 reversed DZ-50-induced MET by antagonizing the drug-induced decrease of nuclear IGFBP3. Furthermore, co-culture with CAFs promoted prostate cancer epithelial cell invasion, an effect that was significantly inhibited by DZ-50. Our findings demonstrate that the lead compound, DZ-50, inhibited the invasive properties of prostate cancer epithelial cells by targeting IGFBP3 and mediating EMT conversion to MET. This study integrated the mechanisms underlying the effect of DZ-50 and further supported the therapeutic value of this compound in the treatment of advanced metastatic prostate cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.