Upregulation of ECT2 is associated with transcriptional program of cancer stem cells and predicts poor clinical outcome in gastric cancer.

Gastric cancer remains the third leading cause of cancer-associated mortality worldwide. The identification of prognostic indicators that are associated with clinical characteristics is urgently required. The aim of the present study was to determine the involvement of epithelial cell transforming 2 (ECT2) in gastric cancer. The results of the present study demonstrated that ECT2 expression was upregulated in human gastric cancer samples. Furthermore, high ECT2 expression was associated with advanced Tumor-Node-Metastasis stage and deeper tumor invasion. ECT2 upregulation was further confirmed in several independent publicly available clinical cohorts from the Gene Expression Omnibus database. In addition, patients with gastric cancer, with high ECT2 expression exhibited a significantly shorter overall survival time than those with low ECT2 expression, and Cox regression analysis demonstrated that ECT2 expression was an independent prognostic marker for overall survival time. Characterization of the transcriptome profiles of ECT2 upregulated gastric tumors indicated that ECT2 upregulation may be associated with transcriptional features of cancer stem cells (CSCs). Additionally, BUB1 mitotic checkpoint serine/threonine kinase and E2F transcription factor 7, two genes previously reported to account for the functionality of CSCs, were strongly enriched in ECT2High gastric cancer samples. Taken together, the results of the present study suggest that ECT2 may serve as a novel marker for CSCs and may be a potential prognostic indicator in gastric cancer.

Steroidal alkaloid solanine A from Solanum nigrum Linn. exhibits anti-inflammatory activity in lipopolysaccharide/interferon γ-activated murine macrophages and animal models of inflammation.

Solanine A is a novel steroidal alkaloid isolated from Solanum nigrum Linn., a medicinal and edible plant which is widely used for treating various inflammatory diseases. In this study, we found that solanine A markedly suppressed the production of nitric oxide (NO) and prostaglandin E2 (PGE2) in lipopolysaccharide/interferon-γ (LPS/IFNγ)-stimulated RAW264.7 cells, and attenuated xylene, carrageenan and agar-induced inflammation in mice. The mRNA levels of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX2), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and -1ß (IL-1ß), as well as C-X-C motif chemokine ligand-9 (CXCL9), were significantly decreased by solanine A. Furthermore, solanine A also suppressed LPS/IFNγ-induced protein expression of iNOS and COX2. Mechanistically, solanine A inhibited the nuclear translocation of nuclear factor-κB (NF-κB) through the prevention of NF-κB p65 and inhibitory κB-α (IκBα) phosphorylation and IκBα degradation, and it also suppressed activation of extracellular regulated protein kinases (ERK), signal transducers and activators of transcription-1 (STAT1) and serine/threonine protein kinase Akt in LPS/IFNγ-stimulated RAW264.7 macrophages and agar-induced granuloma model in mice. Taken together, solanine A exhibits a potent anti-inflammatory activity in LPS/IFNγ- activated macrophages and animal models of inflammation through inhibition of NF-κB, ERK1/2, Akt and STAT1 signaling pathways, suggesting that solanine A may be a valuable leading compound in the treatment of inflammatory diseases.

Horizontal gene transfer events reshape the global landscape of arm race between viruses and homo sapiens.

Horizontal gene transfer (HGT) drives the evolution of recipient organism particularly if it provides a novel function which enhances the fitness or its adaption to the environment. Virus-host co-evolution is attractive for studying co-evolutionary processes, since viruses strictly replicate inside of the host cells and thus their evolution is inexorably tangled with host biology. HGT, as a mechanism of co-evolution between human and viruses, has been widely documented, however, the roles HGT play during the interaction between human and viruses are still in their infancy. In this study, we performed a comprehensive analysis on the genes horizontally transferred between viruses and their corresponding human hosts. Our study suggests that the HGT genes in human are predominantly enriched in immune related GO terms while viral HGT genes are tend to be encoded by viruses which promote the invasion of immune system of hosts. Based on our results, it gives us a hint about the evolution trajectory of HGT events. Overall, our study suggests that the HGT between human and viruses are highly relevant to immune interaction and probably reshaped the arm race between hosts and viruses.