ArticleBMC cancer2025
KIF20A as a driver of anti-PD-1 resistance via PD-L1 downregulation in NSCLC: a biomarker validation and tumor microenvironment analysis.
Article in BMC cancer, 2025. 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
backgroundImmune checkpoint inhibitors targeting PD-1 show limited efficacy in non-small cell lung cancer (NSCLC) due to primary resistance. KIF20A, a cell cycle regulator implicated in chemotherapy resistance, may influence tumor immunity, but its role in anti-PD-1 resistance remains unclear.
methodsWe performed comprehensive bioinformatics analyses to identify KIF20A as a resistance-associated hub gene. Clinical validation was performed in 106 NSCLC patients receiving anti-PD-1 therapy. KIF20A protein expression was assessed by immunohistochemistry (IHC), and tumor microenvironment (TME) profiling was performed using multiplex immunofluorescence (mIHC). Statistical analyses included chi-square tests, Kaplan-Meier survival, Cox regression, and Spearman correlation.
resultsKIF20A was significantly upregulated in NSCLC versus adjacent tissues (63.2% vs. 13.2%, P < 0.001) and associated with lymph node metastasis, poor differentiation, and advanced stage (P < 0.05). High KIF20A expression correlated with primary resistance to PD-1 blockade (P = 0.019) and shorter post-immunotherapy overall survival (HR = 3.40, P = 0.016). Crucially, KIF20A-high tumors exhibited reduced PD-L1⁺ tumor cell density (375.4/mm² vs. 864.8/mm² in KIF20A-low tumors, P = 0.0002), with an inverse correlation (r=-0.249, P = 0.01). Patients with combined KIF20A-high/PD-L1-low expression had the worst prognosis (HR = 6.61, P = 0.030).
conclusionsKIF20A drives primary anti-PD-1 resistance in NSCLC through PD-L1 suppression and independently predicts poor survival. The KIF20A/PD-L1 signature stratifies patient risk, positioning KIF20A as both a prognostic biomarker and a therapeutic target to overcome immunotherapy resistance.
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