The Elevated ASK1 Expression Inhibits Proliferation and Invasion in Gastric Cancer HGC-27 Cells.

This study aimed to evaluate the effects and mechanism of action of ASK1 gene on the growth and migration of gastric cancer (GC) cells. Total RNA was extracted from the gastric cell lines and GC tissues. The expression level of ASK1, and the association between ASK1 expression and clinicopathological characteristics was assessed by real-time polymerase chain reaction. The effects of ASK1 on the proliferation of HGC-27 cells were assessed by the CCK-8 assay. In addition, the effects of ASK1 on the migration of HGC-27 cells were analyzed by the migration assay using transwell chambers. The expression levels of signaling proteins related to cell migration were detected by Western blotting. Although no significant differences were observed in the expression levels of ASK1 between the GC tissue samples and the normal tissue samples (P = 0.241), ASK1 expression correlated with tumor lymph node metastasis (P = 0.008). Furthermore, ASK1 inhibited proliferation and migration of HGC-27 cells. The increase in the expression of ASK1 in HGC-27 cells induced the activation of the JNK and p38 signaling pathways. The findings demonstrated that increased ASK1 expression level inhibited migration and proliferation of HGC-27 gastric cancer cells, whereas the possible mechanism of action may be attributed to the activation of the JNK and p38 signaling pathways. Anat Rec, 301:1815-1819, 2018. © 2018 Wiley Periodicals, Inc.

Tumor necrosis factor-α-induced protein 8-like-2 is involved in the activation of macrophages by Astragalus polysaccharides in vitro.

In previous years, studies have shown that Astragalus polysaccharides (APS) can improve cellular immunity and humoral immune function, which has become a focus of investigations. Tumor necrosis factor­α­induced protein 8­like 2 (TIPE2) is a negative regulator of immune reactions. However, the effect and underlying mechanisms of TIPE2 on the APS­induced immune response remains to be fully elucidated. The present study aimed to examine the role of TIPE2 and its underlying mechanisms in the APS­induced immune response. The production of nitric oxide (NO) was detected in macrophages in vitro following APS stimulation. In addition, the present study interfered with the expression of TIPE2 in macrophages, and examined the production of cytokines, NO and components of the mitogen­activate protein kinase (MAPK) signaling pathway following APS stimulation. The results showed that APS was able to activate macrophages by inducing the production of interleukin (IL)­1ß, tumor necrosis factor (TNF)­α, IL­6 and NO. Furthermore, RAW264.7 cells were stimulated with APS when TIPE2 was silenced, and it was found that the production of TNF­α, IL­6, IL­1ß and NO were upregulated, and the signaling pathway of MAPK was activated. Taken together, these results demonstrated that TIPE2 had an important negative effect on the APS­induced production of inflammatory cytokines and NO via the MAPK signaling pathway.

Inhibitory effects of oligochitosan on TNF-α, IL-1ß and nitric oxide production in lipopolysaccharide-induced RAW264.7 cells.

Oligochitosan has been reported to possess anti-inflammatory properties; however, the mechanism of the antiinflammatory effects of oligochitosan remains unknown. The present study aimed to investigate the expression levels of inflammatory cytokines and the production of nitric oxide (NO), in the nuclear factor (NF)-κB pathway of lipopolysaccharide (LPS)-stimulated RAW264.7 murine macrophages. The results of the present study demonstrated that different concentrations of oligochitosan could significantly lower the levels of NO, tumor necrosis factor (TNF)-α and interleukin (IL)-1ß, released from LPS-stimulated RAW264.7 cells. This was shown to be mediated through inhibiting the activation of the NF-κB pathway. These results demonstrate that oligochitosan may efficiently inhibit inflammation and has the potential to be an effective anti-inflammatory agent.