ArticleScientific reports2021
Translocation of intracellular CD24 constitutes a triggering event for drug resistance in breast cancer.
Article in Scientific reports, 2021. 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, 19 citations in OpenAlex.
- Study on the synergistic efficacy and mechanism of CD24 silencing combined with trastuzumab in HER2-positive breast cancer.Journal of molecular histology · 2026Article
- Silencing CD24 Inhibits Proliferation, Migration, and Chemoresistance in Triple-Negative Breast Cancer Cells.Pharmaceutical research · 2026Article
- Mitoxantrone alters CD24/Siglec-10 expression in malignant brain tumor models.Scientific reports · 2026Article
- Identification of cell adhesion-related subtypes and construction of risk model to predict breast cancer prognostic and immunological properties.World journal of surgical oncology · 2025Article
- Article
- Targeting drug resistance in breast cancer: the potential of miRNA and nanotechnology-driven delivery systems.Nanoscale advances · 2024Review
- LINC00525 enhances ZNF460-regulated CD24 expression through the sponge miR-125a-5p to promote malignant progression of breast cancer.Journal of cancer research and clinical oncology · 2024Article
- From mechanism to therapy: the journey of CD24 in cancer.Frontiers in immunology · 2024Review
- Targeting CD24 as a novel immunotherapy for solid cancers.Cell communication and signaling : CCS · 2023Review
- CD24-associated ceRNA network reveals prognostic biomarkers in breast carcinoma.Scientific reports · 2023Article
- CD24: A Novel Target for Cancer Immunotherapy.Journal of personalized medicine · 2022Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The capacity of tumor cells to shift dynamically between different states could be responsible for chemoresistance and has been commonly linked to the acquisition of stem cell properties. Here, we have evaluated the phenotype switching associated with drug resistance in breast cancer cell lines and cell lineage obtained from Brazilian patients. We have highlighted the role of the cancer stem cell marker CD24 in the dynamics of cell plasticity and the acquirement of drug resistance. We showed that the translocation of CD24 from cytosol to cell membrane is a triggering event for the phenotype change of breast tumor cells exposed to drug stress. Here, we provide evidence that the phenotype switching is due to the presence of a cytosolic pool of CD24. Importantly, the cellular localization of CD24 was correlated with the changes in the dynamics of p38 MAPK activation. A strong and continuous phosphorylation of the p38 MAPK led to the overexpression of Bcl-2 after treatment in persistent cells presenting high density of CD24 on cell membrane. This phenotype enabled the cells to enter in slow-down of cell cycle, after which several weeks later, the dormant cells proliferated again. Importantly, the use of a p38 activity inhibitor sensitized cells to drug treatment and avoided chemoresistance.
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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.