AURKA Enhances Antitumor Immunity by Activating CD4+ T Cell Proliferation in Colorectal Cancer.
1/5 보강
[INTRODUCTION] Colorectal cancer (CRC) ranks third globally in cancer incidence.
- HR 0.44
APA
Xu Y, Wang W, et al. (2025). AURKA Enhances Antitumor Immunity by Activating CD4+ T Cell Proliferation in Colorectal Cancer.. Cancer investigation, 43(9), 740-757. https://doi.org/10.1080/07357907.2025.2559403
MLA
Xu Y, et al.. "AURKA Enhances Antitumor Immunity by Activating CD4+ T Cell Proliferation in Colorectal Cancer.." Cancer investigation, vol. 43, no. 9, 2025, pp. 740-757.
PMID
40995659 ↗
Abstract 한글 요약
[INTRODUCTION] Colorectal cancer (CRC) ranks third globally in cancer incidence. Aurora Kinase A (AURKA) critically regulates tumor proliferation and microenvironment, yet its dual CRC roles remain unclear.
[METHODS] We integrated bulk RNA-seq, scRNA-seq, and 10x Visium spatial transcriptomics to profile AURKA. Immune infiltration was assessed via CIBERSORT/ssGSEA. Clinical validation used IHC/HE staining. Immunotherapy associations were tested in ICB cohorts and murine models.
[RESULTS] Pan-cancer analysis showed CRC-specific AURKA prognostic value ( < 0.05). High AURKA correlated with prolonged OS (median 68 vs 42 months; log-rank = 0.034), conventional adenocarcinoma ( < 0.001), left-sided tumors ( < 0.001), and absent perineural invasion ( = 0.041). Pathway analyses linked AURKA to cell cycle (G2/M checkpoint) and immune pathways (IL-2/STAT5). Spatial transcriptomics identified peritumoral niches (clusters 6/7/12) co-expressing AURKA, CD4, MKI67, and immune-activation markers (HLA-DRB1, CXCL10). IHC confirmed AURKA-CD4 + T-cell correlation (R = 0.66, < 0.05). scRNA-seq revealed AURKA dominance in proliferating T cells. High AURKA predicted anti-PD-1 response (HR = 0.44, = 0.003) and CD4+ memory T-cell expansion in murine models.
[CONCLUSION] AURKA dually regulates tumor proliferation and immune engagement. Its spatial enrichment in T-cell niches supports its use as an immunotherapy biomarker.
[METHODS] We integrated bulk RNA-seq, scRNA-seq, and 10x Visium spatial transcriptomics to profile AURKA. Immune infiltration was assessed via CIBERSORT/ssGSEA. Clinical validation used IHC/HE staining. Immunotherapy associations were tested in ICB cohorts and murine models.
[RESULTS] Pan-cancer analysis showed CRC-specific AURKA prognostic value ( < 0.05). High AURKA correlated with prolonged OS (median 68 vs 42 months; log-rank = 0.034), conventional adenocarcinoma ( < 0.001), left-sided tumors ( < 0.001), and absent perineural invasion ( = 0.041). Pathway analyses linked AURKA to cell cycle (G2/M checkpoint) and immune pathways (IL-2/STAT5). Spatial transcriptomics identified peritumoral niches (clusters 6/7/12) co-expressing AURKA, CD4, MKI67, and immune-activation markers (HLA-DRB1, CXCL10). IHC confirmed AURKA-CD4 + T-cell correlation (R = 0.66, < 0.05). scRNA-seq revealed AURKA dominance in proliferating T cells. High AURKA predicted anti-PD-1 response (HR = 0.44, = 0.003) and CD4+ memory T-cell expansion in murine models.
[CONCLUSION] AURKA dually regulates tumor proliferation and immune engagement. Its spatial enrichment in T-cell niches supports its use as an immunotherapy biomarker.
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