ArticleTranslational cancer research2024
B7-H3 promotes proliferation and migration of lung cancer cells by modulating PI3K/AKT pathway via ENO1 activity.
Article in Translational cancer research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 5 citations in OpenAlex.
- Lactobacillus plantarum-derived indole-3-lactic acid inhibits prostate cancer progression through ASF1B/ENO1 axis and remodels the tumor microenvironment to enhance anti-PD-1 therapy.Molecular biomedicine · 2026Article
- ENO1 as an Immunoregulatory Hub in Cancer: Mechanisms and Translational Implications.Biomolecules · 2026Review
- Enolase 1: A paradigm of metabolic enzyme moonlighting in tumorigenesis (Review).International journal of oncology · 2026Review
- A cascade via CD276/PI3K/SIRT1/E-Cad in overcoming contact inhibition of proliferation in hepatocellular carcinoma cells.Molecular and clinical oncology · 2026Article
- In-depth exploration of programmed cell death-related subtypes and development of a prognostic signature model in lung adenocarcinoma.Scientific reports · 2025Article
- Role of ENO1 and its targeted therapy in tumors.Journal of translational medicine · 2024Review
- O-GlcNAcylation: Crosstalk between Hemostasis, Inflammation, and Cancer.International journal of molecular sciences · 2024Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: B7-H3 (CD276) is overexpressed in diverse malignant tumors and plays critical roles in tumorigenesis and metastasis. However, the mechanism of B7-H3 in lung cancer remains unclear. This study aimed to explore the mechanism of interaction between B7-H3 and α-enolase (ENO1) in lung cancer progression. Methods: Tumor Immune Estimation Resource 2.0 (TIMER 2.0) and Gene Expression Profiling Interactive Analysis 2 (GEPIA 2) databases were used to analyze the B7-H3 messenger RNA (mRNA) expression levels in lung cancer. The Kaplan-Meier (KM) plotter was used to analyze the correlation between B7-H3 and prognosis. Immunoprecipitation and glutathione S-transferase (GST) pull-down were used to verify the B7-H3 and ENO1 interaction. Cell counting kit-8 (CCK-8) and wound healing assays were used to investigate the effect of B7-H3 on the lung cancer growth. Results: Based on the public databases, the analysis showed that B7-H3 mRNA expression levels were up-regulated and correlated with patient prognosis in lung cancer. By using B7-H3 gain and off cell model, we concluded that B7-H3 overexpression promoted proliferation and migration of SBC5 cells. Subsequently, we found that both B7-H3 and ENO1 knockdown could inhibit cell proliferation and migration, in the meanwhile, and the phosphorylation levels of PI3K-p85α, and AKT were significantly reduced. Interestingly, we determined that B7-H3 regulated ENO1 activity rather than changing its expression levels. Furthermore, we used an AP-III-a4 to block ENO1 activity in the experiments, which attenuated the roles of B7-H3 not only on phosphorylation levels of those molecules, but also on cell growth and migration. Conclusions: B7-H3 directly interacts with ENO1 in lung cancer cells. B7-H3 can promote proliferation and migration of lung cancer cells by modulating PI3K/AKT pathway via ENO1 activity.
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