Morbidity and mortality owing to hepatocellular carcinoma (HCC), the most common primary liver cancer, has increased in recent years. Curcumin is a polyphenol compound that has been demonstrated to exert effective antiangiogenic, anti-inflammatory, antioxidant, and antitumor effects. However, its clinical effects in HCC remain elusive. The main aim of the present study was to determine the antiangiogenic effects of curcumin in HCC. H22HCC cells were treated with different concentrations of curcumin in vitro. In addition, a mouse xenograft model was used and analyzed for expression levels of vascular endothelial growth factor (VEGF) protein and proteins of the phosphoinositide 3-kinase (PI3K)/AKT serine/threonine kinase 1 (AKT) signaling pathway. Curcumin treatment inhibited H22 cell proliferation and promoted H22 cell apoptosis in a dose-dependent manner in vitro. In addition, curcumin treatment inhibited tumor growth in vivo at the concentrations of 50 and 100 mg/kg. Furthermore, curcumin treatment significantly decreased VEGF expression and PI3K/AKT signaling. The present findings demonstrated that curcumin inhibited HCC proliferation in vitro and in vivo by reducing VEGF expression.

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Background: Liver fibrosis or cirrhosis is associated with the dismal prognosis of hepatocellular carcinoma (HCC), and it might also be involved in intrahepatic cholangiocarcinoma (ICC). The effect of hepatic fibrosis on the survival of ICC patients is still unclear. This study aims to explore whether liver fibrosis impacts the overall survival (OS) and disease-specific survival (DSS) of ICC patients. Methods: Data of 729 eligible ICC patients receiving different therapies from the Surveillance, Epidemiology, and End Results database (2004-2015) were analyzed. Unmatched, propensity score-matched, and propensity scoreweighted cohorts were used to investigate the relationships of different fibrosis scores (low fibrosis score vs. high fibrosis score) and survival. A Cox regression and Kaplan-Meier curves were used to explore the influence of fibrosis score on patients' survival. Stratified analyses based on treatment modality were conducted to compare the survival difference in ICC patients with different fibrosis scores. Results: Before matching, the one-, three-, and five-year OS were 50.9, 28.0, and 16.1% in the low fibrosis score group (n = 465) and 39.3, 20.1, and 8.0% in the high fibrosis score group (n = 264) (P < 0.001), respectively. After propensity score matching, the one-, three-, and five-year OS were 45.0, 26.0, and 10.2% in the low fibrosis score group and 36.0, 8.1, and 2.3% in the high fibrosis score group (P = 0.008), respectively. The multivariate Cox regression results showed that a high fibrosis score was an independent risk factor of OS. Additionally, patients with high fibrosis scores achieved low DSS after matching (P = 0.032). The survival benefits of the low fibrosis score group were consistent across treatment cohorts. Conclusions: High fibrosis scores were associated with poor clinical outcomes of ICC patients receiving different common therapies.

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