Research Paper Volume 12, Issue 14 pp 14391—14405
The cross-talk between DDR1 and STAT3 promotes the development of hepatocellular carcinoma
Figure 6. Downregulation of DDR1 inhibits HCC progression by regulating STAT3 in nude mice. Stable si-DDR1 or si-NC transfected SNU-182 cells were constructed (A) (n = 6, *p<0.05), and were subcutaneously injected into the right flanks of the nude mice. 1 week later, we injected lentivirus packaged STAT3 into tumors. (B) Tumor weight was determined in the isolated tumors from the nude mice (n = 4, *p<0.05). (C) Immunohistochemical staining of Ki67 used to determine cell proliferation (n = 4, *p<0.05 vs si-NC, #p<0.05 vs si-DDR1). (D) Western blot analyzed the protein level of DDR1, p-STAT3 and STAT3 in tumors (n = 4, *p<0.05 vs si-NC, #p<0.05 vs si-DDR1). qRT-PCR (E) and western blot (F) were used to test the expression of EMT related genes: Vimentin, N-cadherin and E-cadherin (n = 4, *p<0.05 vs si-NC, #p<0.05 vs si-DDR1). (G) The protein expression of glutamine metabolism related genes: GLUD1, GLS1 and SLC1A was determined by western blot (n = 4, *p<0.05 vs si-NC, #p<0.05 vs si-DDR1). (H) Stable si-DDR1 or si-NC transfected SNU-182 cells was intraperitoneally injected into mice, and lentivirus packaged STAT3 was injected into mice through tail vein 3 days later. Lungs were taken out and tumor numbers were calculated 4 weeks later.