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.
BackgroundWe aimed to analyze the clinical characteristics and prognostic features of Chinese patients with relatively late-onset neuromyelitis optica spectrum disorder (RLO-NMOSD>40 years of age at disease onset), compared with patients with relatively early onset NMOSD (REO-NMOSD, ≤ 40 years of age at disease onset).MethodsWe retrospectively reviewed the medical records of patients with NMOSD in central China (with disease courses longer than 3 years) between January 2012 and January 2021. We further analyzed the clinical and prognostic differences between patients with REO-NMOSD and RLO-NMOSD.ResultsA total of 71 patients were included in this study. The results showed that 39 (54.9%) of the patients had RLO-NMOSD. The patients with RLO-NMOSD had higher expanded disability status scale (EDSS) scores than patients with REO-NMOSD at the initial (5.0 vs. 3.0, p = 0.01), 3-month (4.0 vs. 2.5, p = 0.001), 1-year (4.0 vs. 2.5, p = 0.003), 3rd-year (3.5 vs. 3.0, p = 0.0017), and final follow-up (4.0 vs. 2.5, P = 0.002) time points. The EDSS scores of visual function were 2.0 (1.0–3.0) in REO-NMOSD and 3.0 (2.0–3.0) in RLO-NMOSD (p = 0.038) at the final follow-up time point. The locations of spinal cord lesions at transverse myelitis (TM) onset were prone to cervical cord in patients with REO-NMOSD. There were no between-group treatment differences. The risk of requiring a cane to walk (EDSS score of 6.0) increased as the age of disease onset increased: for every 10-year increase in the age of disease onset, the risk of needing a cane to walk increased by 65% [hazard ratio (HR) = 1.65, 95% CI 1.15–2.38, p = 0.007]. Another significant predictor identified in the multivariate analysis was annualized relapse rate (ARR) (HR = 2.01, 95% CI 1.09–3.71, p = 0.025). In addition, we observed a positive correlation between age at onset and EDSS scores at the final follow-up (Spearman's r = 0.426, p < 0.0001) time point. EDSS scores at different periods were significantly different between patients with RLO-NMOSD and REO-NMOSD with anti-aquaporin-4 (AQP4) IgG positive.ConclusionThe patients with RLO-NMOSD developed more severe disabilities than patients with REO-NMOSD at a variety of time periods. All of the patients may experience recurrent aggravated symptoms after their first year, with only patients with REO-NMOSD partly recovering from the 3rd year. The age at onset and ARR were the main predictors of outcomes.
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