Haagensenmccall6677

Colon cancer is the second leading cause of cancer‑related mortality worldwide, and the prognosis of advanced colon cancer has remained poor in recent years. Galectin‑9 (Gal‑9) is a tandem‑repeat type galectin that has recently been shown to exert antiproliferative effects on various types of cancer cells. The present study aimed to assess the effects of Gal‑9 on human colon and colorectal cancer cells in vitro and in vivo, as well as to evaluate the microRNAs (miRNAs/miRs) associated with the antitumor effects of Gal‑9. We examined the ability of Gal‑9 to inhibit cell proliferation via apoptosis, and the effects of Gal‑9 on cell cycle‑related molecules in various human colon and colorectal cancer cell lines. In addition, Gal‑9‑mediated changes in activated tyrosine kinase receptors and angiogenic molecules were assessed using protein array chips in colon and colorectal cancer cells. Moreover, miRNA array analysis was performed to examine Gal‑9‑induced miRNA expression profiles. We also elucidated if Gal‑9 inhibited tumor growth in a murine in vivo model. We found that Gal‑9 suppressed the cell proliferation of colon cancer cell lines in vitro and in vivo. Our data further revealed that Gal‑9 increased caspase‑cleaved keratin 18 levels in Gal‑9‑treated colon cancer cells. In addition, Gal‑9 enhanced the phosphorylation of ALK, DDR1, and EphA10 proteins. Furthermore, the miRNA expression levels, such as miR‑1246, miR‑15b‑5p, and miR‑1237, were markedly altered by Gal‑9 treatment in vitro and in vivo. In conclusion, Gal‑9 suppresses the cell proliferation of human colon cancer by inducing apoptosis, and these findings suggest that Gal‑9 can be a potential therapeutic target in the treatment of colon cancer.Following the publication of the above paper, a concerned reader drew to the Editor's attention that a number of figures (specifically, Figs. 6, 8, 9, 10 and 12) contained apparent anomalies, including repeated patternings of data within the same figure panels. After having conducted an independent investigation in the Editorial Office, the Editor of Oncology Reports has determined that this paper should be retracted from the Journal on account of a lack of confidence concerning the originality and the authenticity of the data. The authors were asked for an explanation to account for these concerns, but the Editorial Office never received any reply. The Editor regrets any inconvenience that has been caused to the readership of the Journal. [the original article was published in Oncology Reports 36 324‑332, 2016; DOI 10.3892/or.2016.4833].Lung cancer is one of the most common types of cancer in the world, resulting in numerous cancer‑associated deaths. The properties of cancer stem cells (CSCs) are important for the initiation and deterioration of lung cancer. Schisandrin B (SchB), an active compound extracted from Schisandra chinensis, exerts anticancer effects in various malignancies, including lung cancer. Nevertheless, the potential of SchB in epithelial‑mesenchymal transition (EMT) and CSC features of large‑cell lung cancer remains unclear. The present study established cancer stem‑like cells derived from large‑cell lung cancer cells, NCI‑H460 and H661, and revealed that SchB inhibited the viability of cancer stem‑like cells at concentrations of ≥40 µmol/l. Moreover, SchB prominently inhibited cell migration, invasion and EMT. Sphere‑forming assays and western blotting demonstrated that the stemness of cancer stem‑like cells was alleviated by SchB treatment. Mechanistically, the current findings revealed that SchB contributed to the suppression of the NF‑κB and p38 MAPK signaling pathways. Notably, further results revealed that the malignant behaviors of NCI‑H460‑CSCs induced by the activation of the NF‑κB and p38 MAPK signaling pathways were suppressed by SchB treatment. Consistently, the inhibitory role of SchB in EMT and CSC activities, as well as in the activation of the NF‑κB and p38 MAPK signaling pathways, was confirmed in vivo. In conclusion, the present study demonstrated that SchB exerted inhibitory effects on large‑cell lung cancer cells via targeting the NF‑κB and p38 MAPK signaling pathways, suggesting that SchB may act as a potential therapeutic drug for large‑cell lung cancer.The journey of cancer cells from a primary tumor to distant sites is a multi‑step process that involves cellular reprogramming, the breaking or breaching of physical barriers and the preparation of a pre‑metastatic niche for colonization. The loss of adhesion between cells, cytoskeletal remodeling, the reduction in size and change in cell shape, the destruction of the extracellular matrix, and the modification of the tumor microenvironment facilitate migration and invasion into surrounding tissues. The promotion of vascular leakiness enables intra‑ and extravasation, while angiogenesis and immune suppression help metastasizing cells become established in the new site. Tumor‑derived exosomes have long been known to harbor microRNAs (miRNAs or miRs) that help prepare secondary sites for metastasis; however, their roles in the early and intermediate steps of the metastatic cascade are only beginning to be characterized. The present review article presents a summary and discussion of the miRNAs that form part of colorectal cancer (CRC)‑derived exosomal cargoes and which play distinct roles in epithelial to mesenchymal plasticity and metastatic organotropism. First, an overview of epithelial‑to‑mesenchymal transition (EMT), metastatic organotropism, as well as exosome biogenesis, cargo sorting and uptake by recipient cells is presented. Lastly, the potential of these exosomal miRNAs as prognostic biomarkers for metastatic CRC, and the blocking of these as a possible therapeutic intervention is discussed.The toxicity of chloroacetamide herbicide in embryo development remains unclear. Acetochlor (AC) is a chloroacetamide that metabolizes into 2‑ethyl‑6‑methyl-2-chloroacetanilide (CMEPA) and 6‑ethyl‑o‑toluidine (MEA). The present study determined the potential effect of AC and its metabolites on embryo development. Both HepG2 cells and zebrafish embryos were exposed to AC, CMEPA and MEA in the presence or absence of co‑treatment with anti‑reactive oxygen species (ROS) reagent N‑acetylcysteine. this website The generation of ROS, levels of superoxide dismutase (SOD) and glutathione (GSH) in HepG2 cells and lactate dehydrogenase (LDH) leakage from HepG2 cells were investigated. The effects of AC, CMEPA and MEA on DNA breakage, MAPK/ERK pathway activity, viability and apoptosis of HepG2 cells were examined by comet assay, western blotting, MTT assay and flow cytometry, respectively. Levels of LDH, SOD and GSH in zebrafish embryos exposed to AC, CMEPA and MEA were measured. The hatching and survival rates of zebrafish embryos exposed to AC, CMEPA and MEA, were determined, and apoptosis of hatched fish was investigated using acridine orange staining.