ArticleScientific reports2017
A novel spontaneous model of epithelial-mesenchymal transition (EMT) using a primary prostate cancer derived cell line demonstrating distinct stem-like characteristics.
Article in Scientific reports, 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.
- NASP implication in the androgen receptor associated with castration resistance in prostate cancer.Cell communication and signaling : CCS · 2025Article
- Exosome-mediated modulation of radioresistance: The radiation-induced bystander effect in prostate cancer cells.PloS one · 2025Article
- Article
- Update on Epithelial-Mesenchymal Plasticity in Cancer Progression.Annual review of pathology · 2024Review
- Engineering principles for rationally design therapeutic strategies against hepatocellular carcinoma.Frontiers in molecular biosciences · 2024Review
- NKX3.1 Expression Contributes to Epithelial-Mesenchymal Transition of Prostate Cancer Cells.ACS omega · 2023Article
- The epithelial-mesenchymal plasticity landscape: principles of design and mechanisms of regulation.Nature reviews. Genetics · 2023Review
- Immunostaining protocol for infiltrating brain cancer spheroids for light-sheet imaging.PloS one · 2023Article
- Prediction of Biochemical Recurrence Based on Molecular Detection of Lymph Node Metastasis After Radical Prostatectomy.European urology open science · 2022Article
- Presence of spontaneous epithelial-mesenchymal plasticity in esophageal cancer.Biochemistry and biophysics reports · 2022Article
- Impact of Circadian Rhythms on the Development and Clinical Management of Genitourinary Cancers.Frontiers in oncology · 2022Review
- Twelfth Annual ENBDC Workshop: Methods in Mammary Gland Biology and Breast Cancer.Journal of mammary gland biology and neoplasia · 2021Article
- Overview of Evidence-Based Chemotherapy for Oral Cancer: Focus on Drug Resistance Related to the Epithelial-Mesenchymal Transition.Biomolecules · 2021Review
- Cancer-associated cells release citrate to support tumour metastatic progression.Life science alliance · 2021Article
- Loss of the Metastasis Suppressor NME1, But Not of Its Highly Related Isoform NME2, Induces a Hybrid Epithelial-Mesenchymal State in Cancer Cells.International journal of molecular sciences · 2021Article
- Emerging Concepts of Hybrid Epithelial-to-Mesenchymal Transition in Cancer Progression.Biomolecules · 2020Review
- A small natural molecule CADPE kills residual colorectal cancer cells by inhibiting key transcription factors and translation initiation factors.Cell death & disease · 2020Article
- β2-Adrenergic Signalling Promotes Cell Migration by Upregulating Expression of the Metastasis-Associated Molecule LYPD3.Biology · 2020Article
- Structural Studies of Epithelial Mesenchymal Transition Breast Tissues.Scientific reports · 2020Article
- New Insights Into the Role of Phenotypic Plasticity and EMT in Driving Cancer Progression.Frontiers in molecular biosciences · 2020Review
Corrections and comments
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Authors and funding
8 authors.
Funding
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Abstract
Cells acquire the invasive and migratory properties necessary for the invasion-metastasis cascade and the establishment of aggressive, metastatic disease by reactivating a latent embryonic programme: epithelial-to-mesenchymal transition (EMT). Herein, we report the development of a new, spontaneous model of EMT which involves four phenotypically distinct clones derived from a primary tumour-derived human prostate cancer cell line (OPCT-1), and its use to explore relationships between EMT and the generation of cancer stem cells (CSCs) in prostate cancer. Expression of epithelial (E-cadherin) and mesenchymal markers (vimentin, fibronectin) revealed that two of the four clones were incapable of spontaneously activating EMT, whereas the others contained large populations of EMT-derived, vimentin-positive cells having spindle-like morphology. One of the two EMT-positive clones exhibited aggressive and stem cell-like characteristics, whereas the other was non-aggressive and showed no stem cell phenotype. One of the two EMT-negative clones exhibited aggressive stem cell-like properties, whereas the other was the least aggressive of all clones. These findings demonstrate the existence of distinct, aggressive CSC-like populations in prostate cancer, but, importantly, that not all cells having a potential for EMT exhibit stem cell-like properties. This unique model can be used to further interrogate the biology of EMT in prostate cancer.
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