BackgroundHepatocellular carcinoma (HCC) is characterized by considerable phenotypic and molecular heterogeneity, but the overall survival of HCC patients remains extremely poor. Thus, novel and efficient alternatives to antitumor agents are urgently needed. Pectolinarigenin, a flavonoid compound extract, has been previously reported for the treatment of nasopharyngeal cancer. However, the potential antitumor roles of pectolinarigenin in HCC have not been clearly elaborated. In the present study, we investigated its role in HCC treatment and explored the potential molecular mechanism(s).Materials and methodsHCC cell lines SMMC7721 and PLC5 were cultured and treated with indicated concentrations of pectolinarigenin. For the HCC cell proliferation, after HCC cells were stimulated with indicated concentrations of pectolinarigenin, the cell viability was detected in CCK-8 and colony-forming assays. HCC cell invasion/migration assay was performed by Transwell and wound scratch methods. Additionally, cellular apoptosis and cell cycle arrest analysis was performed with flow cytometric analysis. Finally, the involved underlying signaling pathway, the PI3K/AKT/mTOR/ERK signaling-related molecular markers were detected through Western blot methods with indicated antibodies. Meanwhile, antitumor activity of pectolinarigenin was also assessed in tumor-bearing mice.ResultsThe results indicated that the treatment with pectolinarigenin significantly inhibited cell proliferation and migratory and invasive abilities of SMMC7721 and PLC5 cells in concentration- and time-dependent manner. Meanwhile, pectolinarigenin markedly induced cell apoptosis and G2/M phase arrest in SMMC7721 and PLC5 cells, which was associated with apoptosis- and cell cycle-related protein levels, respectively. Furthermore, pectolinarigenin inhibited PI3K/AKT/mTOR/ERK signaling pathway. It also significantly suppressed HCC tumor growth in vivo.ConclusionPectolinarigenin could suppress the viability and motility and cause apoptosis and G2/M phase arrest in HCC cell lines by inhibiting the PI3K/AKT/mTOR/ERK signaling pathway. This might be an appealing potential therapeutic agent for HCC treatment.
Background: The present study aimed to assess the risk factors of cholesterol and premalignancy in polypoid lesions of the gallbladder (PLGs) and to establish an appropriate treatment strategy. Methods: Data from patients who underwent cholecystectomy at the First Affiliated Hospital, School of Medicine, Zhejiang University, between January 2011 and July 2017, were collected retrospectively. Results: A total of 1561 patients were included in the present study. The cohort comprised of 636 (40.7%) males and 925 (59.3%) females, with a mean age of 49.5 (range 16-88) years; 65.6% (1024/1561) demonstrated cholesterol lesions in this cohort, among which cholesterol polyps accounted for 81.0%. Age younger than 50 years and multiple number of polyps were found to be independent predictive variables for cholesterol lesions (odds ratio (OR) 3.461, 95% confidence interval (CI) 2.058-5.820, P < 0.001 and OR 3.321, 95% CI 1.988-5.547, P < 0.001, respectively). The presence of polyp growth was associated with premalignancy (OR 5.366, 95% CI 1.466-19.637, P = 0.011), and the presence of clinical symptoms indicated benign non-cholesterol lesions (OR 0.368, 95% CI 0.153-0.885, P = 0.026). Conclusion: In the case of patients ≥50 years old with single asymptomatic polyp, cholecystectomy was recommended if the polyp presented growth at a rate above 3-4 mm within 6 months. If not, trimonthly ultrasound follow up was recommended, and clinicians should carefully assess the risk factors for premalignancy in PLGs.
Neuropilin-2 (NRP2) is a single-pass transmembrane glycoprotein and has recently been detected in several human cancer cells. However, its clinical relevance in hepatocellular carcinoma (HCC) remains unclear. This study aimed at evaluating NRP2 expression and clinicopathological significance in HCC patients. Tissue microarray of 190 HCC patients from the First Affiliated Hospital of Zhejiang University was established, and immunohistochemical staining was performed for NRP2. The Kaplan–Meier analysis and Cox proportional hazard model were used to analyze the survival rate. We found that NRP2 expression in HCC was significantly associated with tumor histological degree (P=0.023) and cirrhosis (P=0.040). Furthermore, NRP2-positive HCC patients demonstrated shorter disease-free survival (DFS) and overall survival (OS) than those of NRP2-negative patients. Then, the multivariate Cox analysis showed that hazard ratios of NRP2-positive patients with DFS and OS were 2.167 (95% CI: 1.626, 2.889) and 2.317 (95% CI: 1.548, 3.469), respectively. Our results suggested that NRP2 expression was considered as an independent factor for the prediction of unfavorable prognosis in HCC patients, and we believe that NRP2 could serve as a biomarker of poor prognosis and a novel target in treating HCC tumors.
Background: In the model for end-stage liver disease (MELD) score, renal function was well thought to be associated with the prognosis of liver recipients. Serum cystatin C (CystC)-based equations were considered more accurate for calculating estimated glomerular filtration rate (eGFR) than creatinine (Pcr) based equations. Thus, we aimed to assess the association between eGFR estimated by chronic kidney disease epidemiology collaboration (CKD-EPI)-CystC equation and post-transplantation mortality. Methods: From January 2015 to January 2018, prior to liver transplantation (LT) and other clinical parameters, CystC was collected in all 307 consecutive patients who underwent LT at our center. Patients were divided into four groups according to the Kidney Disease Outcomes Quality Initiative (KDOQI) classification. Results: Based on CKD-EPI-CystC and the KDOQI classification, 117 patients (38.1%) were stage I, 76 (24.8%) were stage II, 85 (27.7%) were stage III, and 29 (9.4%) were stage IV-V. After univariate and multivariate analysis, MELD score [hazard ratio (HR) =1.035; 95% confidence interval (CI),
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