Macrophages are widely distributed innate immune cells that play indispensable roles in the innate and adaptive immune response to pathogens and in-tissue homeostasis. Macrophages can be activated by a variety of stimuli and polarized to functionally different phenotypes. Two distinct subsets of macrophages have been proposed, including classically activated (M1) and alternatively activated (M2) macrophages. M1 macrophages express a series of proinflammatory cytokines, chemokines, and effector molecules, such as IL-12, IL-23, TNF-α, iNOS and MHCI/II. In contrast, M2 macrophages express a wide array of anti-inflammatory molecules, such as IL-10, TGF-β, and arginase1. In most tumors, the infiltrated macrophages are considered to be of the M2 phenotype, which provides an immunosuppressive microenvironment for tumor growth. Furthermore, tumor-associated macrophages secrete many cytokines, chemokines, and proteases, which promote tumor angiogenesis, growth, metastasis, and immunosuppression. Recently, it was also found that tumor-associated macrophages interact with cancer stem cells. This interaction leads to tumorigenesis, metastasis, and drug resistance. So mediating macrophage to resist tumors is considered to be potential therapy.

Gastric cancer is one of the most common cancers and has the highest mortality rate worldwide. It is worthwhile to explore the mechanism of gastric cancer progression. An increasing number of studies have found that non-coding RNAs including miRNA and lncRNA play important roles in gastric cancer progression. This review summarized the role of ectopic miRNA in gastric cancer proliferation, growth, migration, invasion and apoptosis. Meantime, aberrantly expressed miRNA also received a great deal of attention as potential biomarker for gastric cancer diagnosis and therapy. Over the last decade, lncRNA was considered to regulate gastric cancer progression at the transcript and post-transcript level. At the transcript level, lncRNA induced gastric cancer progression by changing chromatin modification and mRNA stabilization to regulate mRNA and miRNA expression. Furthermore, lncRNA regulated gastric cancer progression by completely combining with miRNA to produce ceRNA or promote protein stabilization at the post-transcript level. Greater attention of miRNA and lncRNA in gastric cancer can provide new insight of mechanism of cancer development and may be acted as a new anticancer target.

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Background Previous studies have suggested a link between Helicobacter pylori (H. pylori) and metabolic abnormality. This study aimed at investigating the correlation between H. pylori infection and metabolic abnormality in a general population. Methods All enrolled participants underwent a carbon-13 urea breath test (13C-UBT). For each individual, the following data were collected: age, gender, alanine transaminase (ALT), total protein, albumin, cholesterol, triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), urea nitrogen, creatinine, uric acid, fasting plasma glucose, postprandial blood sugar, nonalcoholic fatty liver disease (NAFLD), and bone mineral density (BMD). Results The study included 1867 (393 females and 1474 males, aged 54.0 ± 9.6 years) people that took a physical examination. There was no significant difference in gender and age between the study participants with and without H. pylori infection. The statistical data are as follows: albumin: P = 0.045, uric acid: P = 0.025, fasting glucose: P = 0.043, and postprandial blood glucose: P = 0.035. In terms of the patients with NAFLD, there were significant differences in ALT and HDL-C between the study participants with and without H. pylori infection. TG (P = 0.048), HDL-C (P = 0.011), and fasting blood glucose (P = 0.018) were significantly different in both groups among individuals who got osteopenia. Conclusion H. pylori infection may be an important factor affecting metabolic abnormality and osteoporosis.