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The present study aimed to determine whether maslinic acid effectively inhibits the proliferation of MKN28 cells, and to investigate the mechanisms underlying its antitumor functions. MKN28 cell viability was evaluated using a Cell Counting Kit-8, cell proliferation was analyzed by a colony formation assay and flow cytometry was used to investigate the rate of apoptosis. Western blot analysis was performed in order to determine the differential expression levels of Janus kinase (JAK), signal transducer and activator of transcription 3 (STAT3) and apoptosis associated proteins B-cell lymphoma 2 (Bcl-2), Bcl-2 associated X protein (Bax) and Bcl-2 associated agonist of cell death (Bad). Interleukin-6 (IL-6) concentration was evaluated using ELISA. IL-6 and anti-IL-6 antibodies were used to investigate the role of IL-6 in MKN28 cells treated with maslinic acid proliferation, and the STAT3 phosphorylation rates. The results demonstrated that maslinic acid treatment significantly reduced cell proliferation, induced apoptosis and was accompanied by a significant decrease in Bcl-2, Bax and Bad expression levels. Maslinic acid treatment also resulted in the downregulation of phosphorylated-STAT3 and JAK2, and significantly inhibited the protein expression of IL-6. Maslinic acid is able to inhibit MKN28 cell proliferation and the phosphorylation of STAT3 by downregulating the expression of IL-6. These results suggest that maslinic acid suppresses the growth of MKN28 cells by inducing apoptosis via its inhibition of the IL-6/JAK/STAT3 signaling cascade. [ABSTRACT FROM AUTHOR]

Novel targeted therapies need to be developed for gastric cancer, the third most common cancer type and the second most common cause of cancer-related mortality in China. Previous studies indicate that angiopoietin (Ang)-2 serves a role in the proliferation, migration, invasion and adhesion of malignant cells. The present study identified, using functional studies, that exogenous expression of miR-218 increased migration of NCI-87 and HGC-27 gastric cancer cells, which coincided with a reduction in the expression of Ang-2. In addition, intratumoral delivery of miR-218 inhibited proliferation and angiogenesis of gastric cancer cells in vivo, with a corresponding decreased in Ang-2 expression. These results indicate that miR-218 serves an important role in gastric cancer tumorigenesis through regulating the expression of Ang-2. Therefore, components of miR-218/Ang-2 signaling could provide novel therapeutic targets for the treatment of gastric cancer. [ABSTRACT FROM AUTHOR]

Chloride intracellular channel 1 (CLIC1) has been demonstrated to be overexpressed in gastric cancer, and elevated CLIC1 expression levels are markedly associated with the processes of tumor cell migration and invasion. However, the regulatory mechanism and signaling pathway underlying these processes have remained to be elucidated. The present study examined the impact of N-acetyl cysteine (NAC), indanyloxyacetic acid (IAA)-94 and SB203580, inhibitors of reactive oxygen species (ROS), as well as CLIC1 and p38 mitogen-activated protein kinase (MAPK) on the migration and invasion of SGC-7901 gastric cancer cells in a hypoxia-reoxygenation (H-R) microenvironment. The results demonstrated that intracellular ROS and CLIC1 levels were increased under H-R conditions, and that functional inhibition of CLIC1 significantly decreased the H-R-elevated ROS generation and p-p38 MAPK levels in SGC-7901 cells, as well as inhibited the migration and invasion of SGC-7901 cells. In addition, the expression levels of MMP-2 and MMP-9 were inhibited by NAC, IAA-94 and SB203580. These results indicated that CLIC1 regulates gastric cancer-cell migration and invasion via the ROS-mediated p38 MAPK signaling pathway. [ABSTRACT FROM AUTHOR]