Fig. 8. Suppression of TKT abrogates HMGA1-induced ESCC tumor growth.
AKR-WT and AKR-HMGA1 overexpression cells (2.5 × 105/mouse) were injected into flanks of C57BL/6 mice by s.c. The second day after seeding the cells, TKT inhibitor OT (300 mg/kg/day) was applied to the mice by gavage. Tumor volumes were monitored for 13 d. A Timeline for the establishment of the syngeneic mouse model and the treatment of OT. B Representative images of tumors formed in C57BL/6 mice (n = 6). C Tumor weights, and D tumor volume in mice treated with or without OT. E–J Immunohistochemical staining and quantitation of paraffin-embedded tissue sections for HMGA1, TKT, cleaved-caspase 3, γ-H2AX, and Ki-67 in tumors from mice treated with or without OT (n = 6). Scale bar, 100 μm. Data are presented as the means ± S.D., and significant differences are indicated as *P < 0.05, **P < 0.01, and ***P < 0.001. K Schematic diagram depicting that HMGA1 promotes ESCC progression by elevating TKT-mediated upregulation of PPP.