Fig. 7

LincRNA-p21 directly binds to STAT3, impeding its cancer-promoting activity in HNSCC. a The chromosomal location of human lincRNA-p21 was shown. b Eight consecutive primers were designed to amplify the full-length human lincRNA-p21 sequence. c HN6 cells were transfected with lincRNA-p21 plasmid and vector for 48 h. RNA immunoprecipitation was used to detect the binding of STAT3 and lincRNA-p21. d HN6 cells were transfected with lincRNA-p21 plasmid and vector for 48 h. RNA immunoprecipitation was used to detect the binding of p-STAT3 and lincRNA-p21. e Biotinylated lincRNA-p21 was incubated with cell lysates, and the eluent and flow-through were detected via western blotting using anti-STAT3 antibody. L: lysate load; FT: flow-through; E: eluate. f The binding of p-STAT3 to the CCND1, MYC, BCL2, MCL1, MMP9, IL6 and IL10 promoters was detected by a chromatin immunoprecipitation assay in HN6 and Cal27 cells after lincRNA-p21 transfection for 48 h. g The binding of STAT3 and Myc or cyclin D1 was determined by an immunoprecipitation assay in HN6 and Cal27 cells after transfection with lincRNA-p21 plasmid for 48 h. h Schematic diagram show that lincRNA-p21 plays a critical role in the p53/lincRNA-p21/JAK2/STAT3 axis promoting malignant disease progression in HNSCC. *: P < 0.05; **: P < 0.01