ArticleCell cycle (Georgetown, Tex.)2018
Oncogenic transformation of normal breast epithelial cells co-cultured with cancer cells.
Article in Cell cycle (Georgetown, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- RAN-S100A10-EGFR axis facilitates papillary thyroid cancer metastasis by PI3K/AKT signaling.Cell death & disease · 2026Article
- Cancer cell plasticity and therapeutic resistance: mechanisms, crosstalk, and translational perspectives.Hereditas · 2025Review
- Improved breast cancer diagnosis using a CA15-3 capture antibody-lectin sandwich assay.Breast cancer research and treatment · 2025Article
- Epithelial cell-related prognostic risk model in breast cancer based on single-cell and bulk RNA sequencing.Heliyon · 2024Article
- Review
- Breast cancer heterogeneity and its implication in personalized precision therapy.Experimental hematology & oncology · 2023Review
- Time interval between the diagnosis of breast cancer and brain metastases impacts prognosis after metastasis surgery.Journal of neuro-oncology · 2022Article
- Contribution of Tumor-Derived Extracellular Vesicles to Malignant Transformation of Normal Cells.Bioengineering (Basel, Switzerland) · 2022Review
- Article
- BF175 inhibits endometrial carcinoma through SREBP-regulated metabolic pathways in vitro.Molecular and cellular endocrinology · 2021Article
- Graphene Quantum Dot-Based Electrochemical Immunosensors for Biomedical Applications.Materials (Basel, Switzerland) · 2019Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The heterogeneity in human breast cancer poses a challenge for effective treatment. Better understanding of tumor initiation and development will help to resolve this problem. Current models explaining intratumoral diversity include cancer stem cells, clonal evolution and cancer cell dedifferentiation and reprogramming. Herein, a new model, cancer transmission, is proposed to explain cancer heterogeneity. We found breast cancer cells (MCF10A.NeuT) were capable of transforming normal mammary epithelial cells (MCF10A). The transformed cells exhibited cancerous properties including enhanced proliferation and migration, loss of apical-basal polarity and depolarized acini structure associated with epithelial-mesenchymal transition (EMT). The transformed MCF10A cells displayed distinct EMT characteristics compared to parental cells. We further showed that cancer cell-secreted factors were sufficient to induce cancerous transformation of normal cells. Furthermore, transformed cells were resistant to radiation treatment, providing new insights into mechanisms underlying therapeutic resistance.
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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.