Extracellular high-mobility group box-1 (HMGB-1) has been implicated in the inflammation response leading to the precancerous lesions of non-small cell lung cancer (NSCLC). However, the role of HMGB-1 in the inflammation response in normal human bronchial epithelial (NHBE) cells and its underlying mechanisms were still not fully understood. In this study, the inflammation response in NHBE cells was stimulated by 2.5, 5, and 10 μg/ml HMGB-1. However, the receptor for advanced glycation end products (RAGE) blocker RAGE-Ab (5 μg/ml) or 10 μM c-Jun N-terminal kinases (JNK) inhibitor SP600125 could inhibit HMGB1-induced the release of inflammation cytokines including TNF-α, IL-8, IL-10, and MCP-1 in a dose-dependent manner. Furthermore, HMGB1-induced RAGE protein expression, JNK and NF-κB activation were attenuated by the pretreatment with RAGE-Ab or JNK inhibitor SP600125 in Western blot analysis. Our data indicated that HMGB-1 induced inflammation response in NHBE cells through activating RAGE/JNK/NF-κB pathway. HMGB-1 could act as a therapeutic target for inflammation leading NHBE cells to the precancerous lesions of NSCLC.

Lung cancer has very high mortality and glycyrrhizin was found to significantly inhibit the growth of lung cancer cells in vitro and tissues in mice. However, the detailed inhibitory role of glycyrrhizin in the growth of lung cancer is still unclear. In this study, we first found that glycyrrhizin inhibited the growth of lung tumor in PDX mice. And high level of HMGB1 promoted the migration and invasion of lung cancer cells, which was suppressed by glycyrrhizin. Moreover, glycyrrhizin reduced the activity of JAK/STAT signaling pathway, which is the upstream regulator of HMGB1. Therefore, this study revealed a potential mechanism by which glycyrrhizin can inhibit the progression of lung cancer.

Background: Single-nucleotide polymorphisms (SNPs) in microRNAs (miRNA) have been shown to be related with susceptibility to several human cancers. We evaluated the associations of rs3746444 in pre-miRNA hsa-mir-499 with the risk of gastric cancer (GC) in the Chinese population. Patients and Methods: The rs3746444 (A>G) SNPs were genotyped in 201 GC and 213 non-cancer subjects in a case-control study by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis. Results: There was no significant overall difference in the genotype distributions of rs3746444 (A>G) SNPs between cases and controls. In the logistic regression analyses, no significantly increased risk of GC was found to be associated with variant genotypes. Conclusion: The rs3746444 (A>G) SNP is not associated with susceptibility to GC in the Chinese population.