ArticleJournal of hepatocellular carcinoma2026
High Expression of Follistatin is a Risk Factor Predicting Poor Overall Survival in Hepatocellular Carcinoma Patients.
Article in Journal of hepatocellular carcinoma, 2026. 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
Background: Hepatocellular carcinoma (HCC) is a malignant tumor originating from hepatocytes, characterized by high mortality rates. Follistatin (FST), an inhibitor of follicle-stimulating hormone, correlates with poor prognosis in some cancers, but its role in HCC is unclear. This study intends to clarify FST's impact on HCC prognosis and clinical characteristics. Materials and Methods: FST expression was compared between HCC and adjacent tissues using Clinical Proteomic Tumor Analysis Consortium (CPTAC) and The Cancer Genome Atlas (TCGA) databases. 78 HCC patients were dichotomized into FST-high and FST-low groups based on the median expression of FST assessed by immunohistochemistry. Kaplan-Meier analysis evaluated recurrence-free (RFS) and overall survival (OS). Univariate/multivariate Cox regression identified OS risk factors; logistic regression analyzed FST's association with clinical features. Results: FST was upregulated in HCC tissues. High FST correlated with Larger tumor size (OR = 2.030, P = 0.025), Microvascular invasion (OR = 1.933, P = 0.037), Elevated AFP (OR = 2.046, P = 0.024). Patients in the FST-high group had shorter mean OS (53.189 ± 6.37 vs. 94.832 ± 7.739 months, P = 0.0084). Multivariate Cox confirmed FST as an independent OS predictor (HR = 3.88, P = 0.0003), alongside tumor size (HR = 4.33, P = 0.0025) and gender (HR = 0.309, P = 0.0421). Conclusion: FST is upregulated in HCC tissues and serves as an independent prognostic factor for poor overall survival. High FST expression was strongly correlated with aggressive clinicopathological features, including larger tumor burden, microvascular invasion (MVI), and elevated AFP.
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