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a rescue experiment. NCAPD3 was highly expressed in LUAD cells, and its overexpression potentiated the proliferation, migration, invasion, and anti-apoptotic capacities of tumor cells, while promoting M2 phenotypic polarization. Mechanistically, NCAPD3 upregulated FOXM1 expression by recruiting E2F1 to the FOXM1 promoter, thereby inducing M2 polarization of macrophages and accelerating malignant progression in LUAD. By interacting with E2F1, NCAPD3 facilitates the binding of E2F1 to the FOXM1 promoter region to activate FOXM1 transcription, thereby accelerating LUAD progression and triggering M2 macrophage polarization.
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Zhang et al. (2026) studied this question.
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