M2 polarization of macrophages is essential for their function in immunologic tolerance, which might promote tumorigenesis. However, the molecular mechanism behind the polarization process is not fully understood. Given that several lines of evidence have suggested that long noncoding RNAs (lncRNAs) could be involved in regulating immune cell differentiation and function, the current study aimed to identify the lncRNAs that specifically modulate M2 macrophage polarization. By utilizing a series of cellbased M2 macrophage polarization models, a total of 25 lncRNAs with altered expression were documented based on lncRNA microarray-based profiling assays. Among them, lncRNA-MM2P was the only lncRNA upregulated during M2 polarization but downregulated in M1 macrophages. Knockdown of lncRNA-MM2P blocked cytokine-driven M2 polarization of macrophages and weakened the angiogenesis-promoting feature of M2 macrophages by reducing phosphorylation on STAT6. Moreover, manipulating lncRNA-MM2P in macrophages impaired macrophagemediated promotion of tumorigenesis, tumor growth in vivo, and tumor angiogenesis. Collectively, our study identifies lncRNA-MM2P as a modulator required for macrophage M2 polarization and uncovers its role in macrophage-promoted tumorigenesis.

No abstract

Resveratrol, a natural polyphenolic phytoalexin, was reported to exert multiple anticancer effects as a traditional Chinese medicine. However, research regarding the anticancer mechanism of resveratrol for the treatment and prevention of gastric cancer has reported conflicting results. In the present study, it was determined that resveratrol inhibited cell viability in a dose-dependent manner in the human gastric cancer cell line BGC823. Cell migration and invasion were suppressed significantly following treatment with 200 µM resveratrol. Additionally, resveratrol inhibited metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) expression, which was overexpressed in gastric cancer cells. Further experiments revealed that MALAT1 knockdown suppressed cell viability, migration, invasion and epithelial-to-mesenchymal transition in BGC823 cells. The present study indicated that resveratrol inhibited migration and invasion in human gastric cancer cells via suppressing MALAT1-mediated epithelial-to-mesenchymal transition, providing novel evidence for understanding the anticancer mechanism of resveratrol.

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<p>Supplementary figures and figure legends</p>