ReviewFrontiers in oncology2014
P-Cadherin Linking Breast Cancer Stem Cells and Invasion: A Promising Marker to Identify an "Intermediate/Metastable" EMT State.
Review in Frontiers in oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
66 citing papers in PubMed, 105 citations in OpenAlex.
- From Luminal to Triple Negative: 3D Spheroids Reveal Molecular and Phenotypic Differences Across Breast Cancer Subtypes.International journal of molecular sciences · 2026Article
- P-cadherin overexpression is associated with early transformation of the Fallopian tube epithelium and aggressiveness of tubo-ovarian high-grade serous carcinoma.Virchows Archiv : an international journal of pathology · 2026Article
- P-cadherin Overexpression Induces Partial Epithelial-to-Mesenchymal Transition and Confers Chemoresistance in Dysplastic Oral Epithelial Cells.Journal of Cancer · 2026Article
- Identification and Validation of Th1-Selective Epitopes Derived from Proteins Overexpressed in Breast Cancer Stem Cells.Vaccines · 2025Article
- Oncolytic bacteria: A revolutionary approach to cancer therapy.Open life sciences · 2025Review
- Cadherin Expression Profiles Define Glioblastoma Differentiation and Patient Prognosis.Cancers · 2024Article
- How important is EMT for cancer metastasis?PLoS biology · 2024Article
- Identification of a comprehensive alternative splicing function during epithelial-mesenchymal transition.iScience · 2023Article
- Polo-like kinase 4 (Plk4) potentiates anoikis-resistance of p53KO mammary epithelial cells by inducing a hybrid EMT phenotype.Cell death & disease · 2023Article
- MicroRNA 133A Regulates Cell Proliferation, Cell Migration, and Apoptosis in Colorectal Cancer by Suppressing CDH3 Expression.Journal of Cancer · 2023Article
- The expression of high mobility group protein 3 (American journal of cancer research · 2023Article
- Inactivation of PTEN and ZFHX3 in Mammary Epithelial Cells Alters Patterns of Collective Cell Migration.International journal of molecular sciences · 2022Article
- Inhibition of L-type voltage-gated calcium channel-mediated CaCell proliferation · 2022Article
- A functional analysis of 180 cancer cell lines reveals conserved intrinsic metabolic programs.Molecular systems biology · 2022Article
- Article
- CYP1B1 Augments the Mesenchymal, Claudin-Low, and Chemoresistant Phenotypes of Triple-Negative Breast Cancer Cells.International journal of molecular sciences · 2022Article
- Exosomes fromCancers · 2022Article
- Cadherin-3 is a novel oncogenic biomarker with prognostic value in glioblastoma.Molecular oncology · 2022Article
- Article
- Drug Combinations: A New Strategy to Extend Drug Repurposing and Epithelial-Mesenchymal Transition in Breast and Colon Cancer Cells.Biomolecules · 2022Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-mesenchymal transition (also known as EMT) is a fundamental mechanism occurring during embryonic development and tissue differentiation, being also crucial for cancer progression. Actually, the EMT program contributes to the dissemination of cancer cells from solid tumors and to the formation of micro-metastasis that subsequently develop into clinically detectable metastases. Besides being a process that is defined by the progressive loss of epithelial cell characteristics and the acquisition of mesenchymal features, EMT has also been implicated in therapy resistance, immune escape, and maintenance of cancer stem cell properties, such as self-renewal capacity. However, the majority of the studies usually neglect the progressive alterations occurring during intermediate EMT states, which imply a range of phenotypic cellular heterogeneity that can potentially generate more metastable and plastic tumor cells. In fact, few studies have tried to identify these transitory states, partly due to the current lack of a detailed understanding of EMT, as well as of reliable readouts for its progression. Herein, a brief review of evidences is presented, showing that P-cadherin expression, which has been already identified as a breast cancer stem cell marker and invasive promoter, is probably able to identify an intermediate EMT state associated with a metastable phenotype. This hypothesis is based on our own work, as well as on the results described by others, which suggest the use of P-cadherin as a promising EMT marker, clearly functioning as an important clinical prognostic factor and putative therapeutic target in breast carcinogenesis.
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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.