ArticleCancer science2010
CD24-dependent MAPK pathway activation is required for colorectal cancer cell proliferation.
Article in Cancer science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
38 citing papers in PubMed, 72 citations in OpenAlex.
- Targeting CD24 Activates Macrophages to Reduce Tumor Burden in Preclinical Models of Solid Tumors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Silencing CD24 Inhibits Proliferation, Migration, and Chemoresistance in Triple-Negative Breast Cancer Cells.Pharmaceutical research · 2026Article
- Exosomes: a potential tool in the diagnosis, prognosis and treatment of patients with colorectal cancer.Future oncology (London, England) · 2025Review
- Piperine Induces Apoptosis and Cell Cycle Arrest via Multiple Oxidative Stress Mechanisms and Regulation of PI3K/Akt and MAPK Signaling in Colorectal Cancer Cells.Antioxidants (Basel, Switzerland) · 2025Article
- Hsp70 regulates CD24 expression and promotes metastasis and invasion of lung cancer via the MAPK/ERK signaling pathway.Frontiers in oncology · 2025Article
- Exploring the Key Signaling Pathways and ncRNAs in Colorectal Cancer.International journal of molecular sciences · 2024Review
- From mechanism to therapy: the journey of CD24 in cancer.Frontiers in immunology · 2024Review
- Targeting CD24 in Cancer Immunotherapy.Biomedicines · 2023Review
- Targeting CD24 as a novel immunotherapy for solid cancers.Cell communication and signaling : CCS · 2023Review
- Identification of an exosome-related signature associated with prognosis and immune infiltration in breast cancer.Scientific reports · 2023Article
- Emerging phagocytosis checkpoints in cancer immunotherapy.Signal transduction and targeted therapy · 2023Review
- Surprising magic of CD24 beyond cancer.Frontiers in immunology · 2023Review
- CD24: A Novel Target for Cancer Immunotherapy.Journal of personalized medicine · 2022Review
- Polysaccharide immunization and colorectal cancer: A systematic review and network meta-analysis.Frontiers in nutrition · 2022Review
- Prospects of antibodies targeting CD47 or CD24 in the treatment of glioblastoma.CNS neuroscience & therapeutics · 2021Review
- Behavioral Characterizing of CD24 Knockout Mouse-Cognitive and Emotional Alternations.Journal of personalized medicine · 2021Article
- Elevated hippocampal CD24 in astrocytes participates in neural regeneration possibly via activating SHP2/ERK pathway after experimental traumatic brain injury in mice.American journal of translational research · 2020Article
- Molecular Mechanism of Tumor Cell Immune Escape Mediated by CD24/Siglec-10.Frontiers in immunology · 2020Review
- Signature mRNA markers in extracellular vesicles for the accurate diagnosis of colorectal cancer.Journal of biological engineering · 2020Article
- Combination of targeting CD24 and inhibiting autophagy suppresses the proliferation and enhances the apoptosis of colorectal cancer cells.Molecular medicine reports · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CD24 is a glycosylphosphatidylinositol-anchored membrane protein reported to be overexpressed in human tumorigenesis and progression. Our purpose was to determine the role of CD24 in the proliferation of colorectal cancer cells and the potential mechanisms in this process. Our data showed that CD24 promoted cell growth and induced activation of extracellular signal-regulated kinases, Raf-1, and p38 mitogen-activated protein kinase. Furthermore, suppression of extracellular signal-regulated kinases and p38 mitogen-activated protein kinase activity by their specific inhibitors, U0126 and SB203580, abrogated CD24-induced proliferation in vitro. By tumorigenicity assay in female BALB/c nude mice, we further demonstrated that CD24 promoted tumor growth in vivo. Immunohistochemical analysis revealed that CD24 expression occurred in 92.5% of human colorectal cancer tissue, and increased with tumor progression. More importantly, the stainings of phospho-extracellular signal-regulated kinases and phospho-p38 mitogen-activated protein kinase were strongly correlated with CD24 expression. Taken together, our data suggest that CD24-dependent extracellular signal-regulated kinases and p38 mitogen-activated protein kinase activations are required for colorectal cancer cell proliferation in vitro and in vivo. The linkage of CD24 and the mitogen-activated protein kinase pathway may unravel a novel mechanism in the regulation of colorectal cancer proliferation.
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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.