Fig 1: Silencing each gene of the m6A signature expression in UCEC inhibits cell proliferation, migration, and invasion in vitro and in vivo. A Western blot analysis of each gene (COL4A4, PXDN, CDKN2A, TIGIT, CHODL, LMO3, KCNJ12, L1CAM, and EPHB1) expression in Ishikawa cells expressing each gene shRNA (shCOL4A4, shPXDN, shCDKN2A, shTIGIT, shCHODL, shLMO3, shKCNJ12, shL1CAM, and shEPHB1). ß-actin is adopted as a loading control. B MTT assays were used to investigate the proliferation rates of the COL4A4, PXDN, CDKN2A, TIGIT, CHODL, LMO3, KCNJ12, L1CAM, EPHB1-silenced Ishikawa cells. C Colony formation assay was used to investigate the proliferation capacity of the COL4A4, PXDN, CDKN2A, TIGIT, CHODL, LMO3, KCNJ12, L1CAM, EPHB1-silenced Ishikawa cells. Representative pictures are shown on the left, and the number of colonies has been counted on the right. D Transwell assay was used to investigate the metastasis capacity of the COL4A4, PXDN, CDKN2A, TIGIT, CHODL, LMO3, KCNJ12, L1CAM, EPHB1-silenced Ishikawa cells. Representative pictures are shown on the left, and the number of metastasis cells has been counted on the right. E Wound healing assay was used to investigate the migration capacity of the COL4A4, PXDN, CDKN2A, TIGIT, CHODL, LMO3, KCNJ12, L1CAM, EPHB1-silenced Ishikawa cells. Representative pictures are shown on the left, and the wound width has been measured on the right. F Macroscopic view of tumor harvested of two indicates treatment groups (n = 4). G Comparison of the tumor weight of two indicated treatment groups at the end-point (n = 4). H Comparison of the growth curve of the tumors of two indicates treatment groups at the each-point (n = 4). Bar graph data are presented as mean ± SEM; *, P < 0.05