ArticleJournal for immunotherapy of cancer2025
Blocking PCSK9 suppresses hepatocellular carcinoma immune escape by decreasing FLI1-mediated SPP1 and PD-L1 expression.
Article in Journal for immunotherapy of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- NAT10 promotes gallbladder cancer progression by remodeling cholesterol metabolism via PCSK9 mRNA acetylation.Cell death discovery · 2026Article
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13 authors.
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Abstract
backgroundProprotein convertase subtilisin/kexin type 9 (PCSK9) is a newly identified immunosuppressive regulator, but its mechanism of suppressing antitumor immunity remains ambiguous. This study aims to uncover the underlying mechanism by which PCSK9 promotes hepatocellular carcinoma (HCC) immune escape and to explore potential intervention strategies.
methodsCo-culture assay assessed the cytotoxicity of CD8
resultsWe found that PCSK9 was highly expressed and correlated with poor survival in patients with HCC. While PCSK9 deficiency did not affect HCC growth in vitro, it significantly enhanced CD8
conclusionsPCSK9 promoted HCC immune escape by upregulating SPP1 and PD-L1 via NOTCH3/FLI1 signaling. CRISPR ABE-mediated PCSK9 deficiency and PCSK9 inhibitor parecoxib may serve as effective strategies to inhibit HCC.
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