Fig. 7
Knockdown of KRT17 inhibits tumor stemness and synergistically enhanced inhibitory effects of cisplatin on of OSCC tumor growth. A KRT17 knockdown (shKRT17) efficiency was determined via KRT17 protein expression by immunoblotting and comparison to the shRNA control (shCon) in C9IV3 cells (left panel). SCID mice were injected with 5 × 105 shCon or shKRT17 C9IV3 cells in right flank, and PBS or cisplatin was administered two times a week. Tumor volumes were measured weekly after transimplantation before tumor excision at day 42. Right panel shows the tumor growth curve of each treatment group. Data are presented as mean ± SD (n = 5, **p < 0.01 and ***p < 0.001). B Excised tumors from the xenograft model was shown at the end of 42 days. C Tumor weights of the excised tumors (**p < 0.01 and ***p < 0.001). D Immunohistochemical staining for protein expressions of KRT17, ITGB4, active β-catenin, CD44 and EGFR in representative tumor excised (Scale bar, 50 μm). E A schematic diagram that depicts a novel signaling mechanism mediated by miR-485-5p/KRT17/integrin/FAK/Src/ERK/β-catenin that contributes to cancer stemness and drug resistance in OSCC