Fig 1: Relative basal expression of RPL17 in diverse CRC cell lines at mRNA (A) or protein (B) level. β-actin protein was included as a loading control.
Fig 2: RPL17 promotes migration and invasion of CRC cells. (A) Representative light microscopy images of migratory or invasive NCsiRNA- or RPL17siRNA-transfected HCT116 cells. The number of migrated or invaded cells was counted and graphed. (B) Representative light microscopy images of migratory or invasive control (vector only) or v-RPL17 #13 cells. (C) Changes in mRNA level of E-cadherin and vimentin in control or v-RPL17 #13 cells. *p < 0.05; **p < 0.01 vs control.
Fig 3: Molecular mechanisms underlying CRC phenotypic changes induced by RPL17 silencing. (A)-(C) Transcriptomic analysis of RPL17 knockdown cells by RNA sequencing. (A) The number of genes dysregulated in HCT116 and/or HT29 cells 48 h after siRNA treatment. (B) A heat map of the 159 genes commonly up- or down-regulated in both HCT116 and HT29 cells (Red, up-regulated; green, down-regulated). (C) IPA network 2 functionally associated with NEK2. (D) Detection of RPL17, NEK2, β-catenin, phospho-ERK, and total ERK in HCT116 and HT29 cells 48 h after siRNA transfection.
Fig 4: Targeting RPL17 increases the sub-G1 population and apoptosis of CRC cells. (A) Changes in cell cycle progression were measured by flow cytometry 48 h after siRNA treatment and is shown in a histogram. (B) The fraction of apoptotic cells was measured by FACS analysis 48 h after siRNA treatment. (C) Protein expression of RPL17, PARP-1, cleaved PARP-1, and pro-caspase 3 in HCT116 and HT29 cells. β-actin was used as a loading control. U, untreated cells.
Fig 5: Schematic diagram illustrating the regulation of RPL17 to exert cancer cell survival and stemness.
Supplier Page from Abcam for Anti-RPL17 antibody