Objective To further investigate the effect of sinomenine (SIN) on TNF-α-induced VCAM-1 expression in human umbilical vein endothelial cells (HUVECs). Methods HUVECs were isolated from freshly collected umbilical cords. Positive control samples were stimulated with TNF-α, but free of SIN. Negative control samples were treated in the same way, but without TNF-α and SIN. Experimental samples were co-cultured with TNF-α and SIN at various concentrations (0.25, 0.5, and 1.0 mol/L), or TNF-α and dexamethasone (Dex) at concentration of 1.0×10-6 mol/L, or TNF-α with Dex (at concentration of 1.0×10-6mol/L) and SIN at different concentrations (0,25, 0.5, and 1.0 mmol/L) (co-treated groups). VCAM-1 expression was detected by flow cytometry (FCM). Results SIN inhibited expression of VCAM-1 in TNF-α-induced HUVECs, the best effect was shown in the 1.0 mmol/L SIN treated group. VCAM-1 decreased more markedly in the co-treated groups. Conclusion SIN inhibits TNF-α-induced VCAM-1 expression on HUVECs in vitro, and SIN maybe synergistic with Dex in inhibiting TNF-α-induced VCAM-1 expression on HUVECs in vitro.

Exosomes are a class of extracellular vesicles that secreted by a variety of cells, with the length of 40-100 nm and a lipid bilayer membrane structure. They are often observed in multiple body fluids and are important mediators in intercellular communication. Several researches demonstrated that exosomes are closely linked to the development, invasion, metastasis, and drug resistance of colorectal cancer (CRC). In this review, the role of CRC-derived exosomes in the pathogenesis, diagnosis, prognosis and treatment of CRC were briefly summarized to provide a strategy for new therapeutic targets in CRC.

Small nucleolar RNAs(snoRNAs) constitute a large group of non-coding RNAs. Canonical snoRNAs contain C/D box and H/ACA box types, with the length of 60-300 nucleotides. They are predominantly engaged in 2′-O-methylation or pseudouridylation of ribosomal RNAs. Mounting evidence supported that snoRNAs were a kind of detectable modulators affecting multiple cell behavior and eventually triggered tumorigenesis. The aberration of snoRNAs could regulate cancer-related signal pathways, expedite degradation of p53 protein and induce self-renewal. Herein, the snoRNAs′ structure and the latest progress of snoRNAs research in malignancy were briefly summarized, hoping to provide a new idea for the discovery of effective therapeutic targets and promising tumor prognosis markers.