ArticleOncotarget2016
The co-stimulatory molecule B7-H3 promotes the epithelial-mesenchymal transition in colorectal cancer.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 80 citations in OpenAlex.
- A cascade via CD276/PI3K/SIRT1/E-Cad in overcoming contact inhibition of proliferation in hepatocellular carcinoma cells.Molecular and clinical oncology · 2026Article
- Multiomic analysis of colorectal adenocarcinoma reveals a new subtype of myofibroblastic cancer-associated fibroblasts that express high levels of B7-H3 and have poor-prognosis value.Journal for immunotherapy of cancer · 2026Article
- Expression profiling of inhibitory immune checkpoints in colorectal cancer stem cells and their association with tumor immunity and immunotherapy biomarkers.Frontiers in immunology · 2026Article
- The role of immune checkpoints in modulating cancer stem cells anti-tumor immune responses: implications and perspectives in cancer therapy.Journal of experimental & clinical cancer research : CR · 2025Review
- Unveiling transcriptional mechanisms of B7-H3 in breast cancer stem cells through proteomic approaches.iScience · 2025Article
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- Dual-Action flavonol carbonized polymer dots spray: Accelerating burn wound recovery through immune responses modulation and EMT induction.Materials today. Bio · 2025Article
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- High CTLA-4 gene expression is an independent good prognosis factor in breast cancer patients, especially in the HER2-enriched subtype.Cancer cell international · 2024Article
- LAG-3 : recent developments in combinational therapies in cancer.Cancer science · 2024Review
- B7-H3 enhances colorectal cancer progression by regulating HB-EGF via HIF-1α.Journal of gastrointestinal oncology · 2024Article
- CD276 promotes epithelial-mesenchymal transition in esophageal squamous cell carcinoma through the TGF-β/SMAD signaling.Clinical & experimental metastasis · 2024Article
- B7-H3 at the crossroads between tumor plasticity and colorectal cancer progression: a potential target for therapeutic intervention.Cancer metastasis reviews · 2024Review
- N6-methyladenosine modification of B7-H3 mRNA promotes the development and progression of colorectal cancer.iScience · 2024Article
- Article
- Dual Inhibition of B7-H3 and EGFR Overcomes Acquired Chemoresistance in Colon Adenocarcinoma.Journal of Cancer · 2024Article
- CD276 Promotes an Inhibitory Tumor Microenvironment in Hepatocellular Carcinoma and is Associated with Poor Prognosis.Journal of hepatocellular carcinoma · 2024Article
- A Comprehensive Study on the Prognostic Value and Clinicopathological Significance of Different Immune Checkpoints in Patients With Colorectal Cancer: A Systematic Review and Meta-Analysis.Current therapeutic research, clinical and experimental · 2024Review
- B7-H3 in glioblastoma and beyond: significance and therapeutic strategies.Frontiers in immunology · 2024Review
- EMT-induced immune evasion: connecting the dots from mechanisms to therapy.Clinical and experimental medicine · 2023Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
B7-H3, first recognized as a co-stimulatory molecule, is abnormally expressed in cancer tissues and is associated with cancer metastasis and a poor prognosis. However, as an initial event of metastasis, the relationship between the Epithelial-Mesenchymal Transition (EMT ) in cancer cells and B7-H3 has still not been investigated. In this study, we first analyzed B7-H3 expression by immunohistochemistry in colorectal cancer tissues. B7-H3 was expressed in the cancer cell membrane and was associated with the T stage of colorectal cancer; it also showed a positive correlation with MMP2 and MMP9 expression in cancer tissues. Over-expression of B7-H3 in SW480 cells allowed cancer cells to invade and metastasize more than the control cells, whereas invasion and metastasis capabilities were decreased after B7-H3 was knocked down in Caco-2 cells. We further showed that B7-H3 down-regulated the expression of E-cadherin and β-catenin and up-regulated N-cadherin and Vimentin expression, implying that B7-H3 promoted the EMT in colorectal cancer cells. We also checked another character of the EMT, the stemness of cancer cells. CD133, CD44 and Oct4 were significantly elevated after the SW480 cells were transfected with B7-H3 and reduced in Caco-2 cells after B7-H3 was inhibited. In subsequent studies, we proved that B7-H3 upregulated the expression of Smad1 via PI3K-Akt. In conclusion, B7-H3 promotes the EMT in colorectal cancer cells by activating the PI3K-Akt pathway and upregulating the expression of Smad1.
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