Fig 2: The expression of RPL31 in gastric cancer (GC). (A) The negative staining in para-carcinoma tissues compared with the positive staining in tissues with different extent of tumor infiltrate. (B) IHC quantitative results revealed the expression of RPL31 in GC. (C) RPL31 expression in normal gastric mucosa cell GES1 and two GC cell lines (AGS and MGC-803), respectively. ***P < 0.001.

Fig 3: RPL31 knockdown reduces proliferation and enhances apoptosis of GC cells. (A) The ability of cell proliferation in shRPL31-harboring and negative groups of AGS and MGC-803 cell lines resulted from Celigo cell counting assay. (B) The percentages of cell apoptosis obtained by flow cytometry in shRPL31-harboring and negative groups of AGS and MGC-803 cell lines. (C) The percentages of experimental cells in each stage in shRPL31-harboring and negative groups of AGS and MGC-803 cell lines. **P < 0.01, ***P < 0.001.

Fig 4: The underlying regulating mechanism of RPL31 in GC cells. (A–B) The comparison of protein levels in shRPL31 and shCtrl groups of MGC-803 cells resulted from Human phospho-kinase array. (C) The changes in expression of Bcl-2, c-Myc, P21, p-Stat3, JAK1 and JAK2 as a result of RPL31 knockdown. Notably, full and non-adjusted images are available in the Supplemental materials folder. *P < 0.05, **P < 0.01, ***P < 0.001.

Fig 5: Depletion of RPL31 imposes restrictions on tumor growth in vivo. (A) The growing volume of transplanted tumor after injecting shRPL31 and shCtrl groups of MGC-803 cells. (B) The fluorescence images and the comparison of total fluorescence intensity of experimental animals between shRPL31 and shCtrl groups. (C) The separated xenograft tumors from experimental animals and the comparison in tumor weight between shRPL31 and shCtrl groups. (D) The representative images of xenograft tumors after KI67 staining. *P < 0.05, ***P < 0.001.