Based on in silico results, ChalcEA with the binding energy of -6.53 kcal/mol could compete better than 4-methyl benzenesulfonamide (-6.43 kcal/mol) as an inhibitor of caspase-3 (PDB 2XYG). ChalcEA has potential since it has three hydrophobic features. These results provided a basis for further study of ChalcEA as an active compound for anticancer therapeutics. Copyright © Hadisaputri et al.Gastric cancers (GCs) may develop in the gastric mucosa after elimination of Helicobacter pylori (H. pylori) using eradication therapy. Cytokine signaling is a key mechanism underlying GC development and progression, and STAT3 signaling may serve a central role in gastritis-associated tumorigenesis. In the present study, suppressor of cytokine signaling 3 (SOCS3) methylation was examined, as an activator of phosphorylated (p-)STAT3 expression in the non-neoplastic gastric mucosa (non-NGM) of patients with early GC. The methylation status of the SOCS3 gene promoter was analyzed using methylation-specific PCR in the non-NGM of patients with or without early GC. Expression levels of p-STAT3 and Ki67 were investigated immunohistochemically in non-NGM with early GC before and after H. pylori eradication. In non-NGM, SOCS3 promoter methylation was detected in 17/51 patients (33.3%) with early GC. In those patients, the non-NGM labeling indices of both Ki67 and p-STAT3 were significantly higher compared with that in patients with early GC without SOCS3 methylation. A significant correlation between Ki67 and p-STAT3 expression levels was demonstrated in the non-NGM of patients with early GC. In patients with early GC without SOCS3 methylation, the labeling indices of both Ki67 and p-STAT3 in non-NGM were significantly reduced after H. pylori eradication, whereas no such change was observed in patients with early GC with SOCS3 methylation. SOCS3 methylation is associated with continuous p-STAT3 overexpression and enhanced epithelial cell proliferation in non-NGM of patients with early GC. Copyright © Fukui et al.Keratin 17 (KRT17) has been demonstrated to be a potential biological marker for the prediction of prognosis in particular types of cancer. The aim of the present study was to investigate the molecular mechanisms underlying the function of KRT17 in the pancreatic cancer (PAC) cell line PANC-1 and the potential of KRT17 as a therapeutic target for PAC. KRT17 expression levels were analyzed using quantitative PCR and compared with histological data using bioinformatics tools in PAC samples and three human PAC cell lines. Cell proliferation was determined using an MTT assay, in addition to cell cycle distribution and apoptosis analysis using flow cytometry, colony formation assay using Giemsa staining and cell motility analysis using a Transwell migration assay. Tumor growth was evaluated in vivo in nude mice. The expression levels of a number of signaling molecules were measured to establish the potential mechanism by which silencing KRT17 expression affected PAC PANC-1 cells. Increased levels of KRT17 expressilts of the present study suggested that KRT17 may be a potential target for the treatment of pancreatic cancer. Copyright © Chen et al.Peroxiredoxin IV (PRDX4) is a multifunctional protein that is involved in cell protection against oxidative injury, regulation of cell proliferation, modulation of intracellular signaling, and the pathogenesis of tumors. We previously conducted a proteomic analysis to investigate tumor-specific protein expression in gastric cancer. The aim of the present study was to investigate whether PRDX4 could be a marker of poor prognosis in patients with gastric cancer.  https://www.selleckchem.com/products/jsh-23.html  Immunohistochemistry was used to validate PRDX4 as a prognostic marker for gastric cancer. Short hairpin RNA (shRNA)-mediated knockdown of PRDX4 expression in AGS cells and MKN28 cells was used for functional studies, and PRDX4 overexpression in PRDX4-depleted cells was used for knock-in studies. Based on immunohistochemistry data, TNM stage and PRDX4 were independent prognostic factors in the Cox proportional hazard model (P less then 0.05). In the survival analysis, the PRDX4-overexpressing group demonstrated significantly worse survival than the PRDX4-underexpression group (P less then 0.01). In vitro, knockdown of PRDX4 expression by shRNA caused a significant decrease in cancer invasion. Conversely, overexpression of PRDX4 in PRDX4-depleted cancer cells promoted migration and invasion. By measuring the expression of EMT-related genes, we found that E-cadherin was increased in shPRDX4 cells compared with control shMKN28 cells, and snail and slug were decreased in shPRDX4-1 cells compared with sh-control cells. Furthermore, the expression levels of these genes could be recovered in rescue experiments. In conclusion, the results of the present study suggested that PRDX4 is a marker of poor prognosis in gastric cancer and that PRDX4 is associated with cancer cell migration and invasion via EMT. Copyright © Park et al.The present study aimed to investigate the probability of cancer-associated mortality of patients with esophageal cancer undergoing intensity-modulated radiation therapy (IMRT), and to establish a competing risk nomogram to predict the esophageal cancer-specific survival (EC-SS) of these patients. A total of 213 patients with EC who underwent IMRT between January 2014 and May 2017 were selected to establish nomograms according to Fine and Gray's competing risk analysis. Predictive accuracy and discriminative ability of the model were determined using the concordance index (C-index), calibration curves and the area under receiver operating characteristic curves. Decision tree analysis was also constructed for patient grouping. With a median follow-up of 19 months (range, 3-50), the 2-year EC-specific mortality (EC-SM) and the non-esophageal cancer specific mortality (NEC-SM) of the cohort were 35.4 and 3.51%, respectively. Furthermore, an elevated 2-year EC-SM was observed in patients with tumor length ≥4.5 cmompeting event for patients with EC with a tumor length ≥4.5 cm. The competing risk nomograms may therefore be considered as convenient individualized predictive tools for cancer-specific survival in patients with EC undergoing IMRT treatment. Copyright © Zhao et al.