ArticleClinical and experimental medicine2025
Prognostic implication of six m6A-modulated genes signature in the ferroptosis for hepatocellular carcinoma patients.
Article in Clinical and experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Mechanism and therapeutic prospects of ferroptosis regulation through m6A in cancer.Frontiers in cell and developmental biology · 2026Review
- Article
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Authors and funding
10 authors.
Funding
Abstract
Hepatocellular carcinoma (HCC) remains one of the most prevalent and lethal malignancies worldwide, with survival rates still falling short of expectations. Emerging evidence highlights the pivotal roles of both m6A methylation and ferroptosis-related genes (FRGs) in HCC progression. However, the prognostic significance of m6A-modulated FRGs remains largely unexplored. In this study, we developed a novel prognostic signature based on m6A-regulated FRGs, identifying six key genes (VEGFA, FANCD2, ZFP69B, EIF2S1, SLC7A11, and SRXN1) through multivariate and LASSO Cox regression analyses. A high m6A-FRGs score was strongly associated with poor prognosis, and multivariate analysis confirmed it as an independent prognostic factor. Notably, the high-risk group exhibited increased expression of immune checkpoint genes and a higher frequency of gene mutations. Functional assays further demonstrated that silencing ZFP69B significantly suppressed liver cancer cell proliferation, migration, and invasion. Clinical validation in 144 HCC samples revealed that elevated ZFP69B expression correlated with worse patient outcomes. Moreover, qPCR analysis confirmed CLSPN and HNRNPR as downstream targets of ZFP69B. Collectively, our findings establish the m6A-FRGs signature as a powerful prognostic tool for HCC and identify ZFP69B as a promising therapeutic target, warranting further investigation.
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