ArticleFrontiers in immunology2026
An anoikis-related gene signature predicts prognosis and immunotherapy response, and identifies CCAR2 as a therapeutic target in triple-negative breast cancer.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Triple-negative breast cancer (TNBC) has poor prognosis, largely due to its high rates of metastasis and recurrence. Anoikis plays a pivotal role in tumor metastasis; however, its role in TNBC remains elusive. Methods: Cox regression analysis was performed on anoikis-related genes (ARGs) to develop a prognostic signature. A clinical nomogram was developed based on the prognostic signatures. Associations of the signature with the immunogenomic landscape and response to targeted therapy and immunotherapy were assessed. Key prognostic genes were identified using random survival forest analysis. To evaluate Cell cycle and apoptosis regulator 2 (CCAR2) expression and its independent prognostic role, we performed RT-qPCR, immunohistochemistry, Kaplan-Meier analysis, and multivariate Cox regression analysis. Results: A six-gene prognostic signature based on ARGs was constructed, stratifying patients into high- and low-risk groups with a significant difference in overall survival. The nomogram achieved good calibration and strong discriminatory accuracy. Additionally, the signature showed significant correlations with the immunogenomic landscape and predicted the response to both targeted therapy and immunotherapy. Random survival forest analysis identified CCAR2 as a key gene. In TNBC, upregulation of CCAR2 independently predicted a higher histological grade, metastasis, and poor overall survival. Its knockdown inhibits cell migration and invasion, suppresses stemness, and induces anoikis. Furthermore, CCAR2 is associated with an immunosuppressive tumor microenvironment in basal-like TNBC, fostering an immune-evasive phenotype that correlates with a poorer predicted response to immunotherapy. Conclusion: We constructed an ARG-based prognostic signature for TNBC and identified CCAR2 as a key metastatic driver that confers anoikis resistance, immune evasion, and stemness. These findings may advance the prognostic stratification of TNBC and could highlight CCAR2 as a potential therapeutic target for TNBC.
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