Fig. 2

LncRNAs potentially modulate tumor metastasis through interacting with tumor immunity. a AFAP1-AS1 might contribute to the apoptosis or deactivation of TILs by increasing PD-1 expression in TILs, which is an immune escape marker, thus leading to immunosuppressant TME and metastasis of NPC. b HOTAIR could integrate with PRC2 as a complex under stimulation of mast cells to suppress AR, and thus increase MMP9 levels and the stem/progenitor cell population, contributing to the metastasis of prostate cancer cells. c Infiltrating macrophages in TME could potentiate invasion of breast cancer in vitro by increasing AKT phosphorylation, thus boosting level of lncRNA UCA1. d LncAGER could attenuate the tumor migration and growth of lung cancer via targeting miR-185, thus reversing the impact of miR-185 on inhibiting AGER expression in lung cancer cells and inducing the anti-tumor effect of human monocytes. lncRNAs: Long noncoding RNAs; AFAP1-AS1: Actin filament associated protein 1 antisense RNA 1; TILs: Tumor infiltrating lymphocytes; PD-1: Programmed death 1; TME: Tumor microenvironment; NPC: Nasopharyngeal carcinoma; HOTAIR: Homeobox transcript antisense RNA; PRC2: Polycomb repressive complex 2; AR: androgen receptor; PCa: prostate cancer; UCA1: Urothelial carcinoma-associated 1; AKT: Protein Kinase B; AGER: advanced glycosylation end-product specific receptor; lncAGER: lncRNA AGER; miR-185: microRNA-185