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. 2023 Jul 14;13(12):4042–4058. doi: 10.7150/thno.84388

Figure 2.

Figure 2

KLF7 fosters HCC metastasis through transcriptionally upregulating TLR4 and PTK2 expression. (A) Differentially-expressed genes between PLC/PRF/5-KLF7 cells and PLC/PRF/5-control cells were detected using A human liver cancer PCR array. (B) The mRNA and protein levels of TLR4 and PTK2 in PLC/PRF/5 cells with KLF7 overexpression or in MHCC97H cells with KLF7 knockdown. (C) Relative luciferase activities of TLR4 and PTK2 promotor reporter plasmids in PLC/PRF/5 cells co-transfected with pCMV-KLF7 or pCMV-Taq. (D-E) Serially truncated/mutated TLR4 or PTK2 promotor constructs were co-transfected with pCMV-KLF7 into PLC/PRF/5 cells for testing luciferase activities. (F-G) ChIP assays showed KLF7 directly bound to the TLR4 and PTK2 promoters in HCC cells and HCC specimens. (H) TLR4 and PTK2 knockdown in KLF7-overexpressing PLC/PRF/5 cells and upregulation in MHCC97H cells with KLF7 knockdown were confirmed by western blot. (I) The migratory and invasive capacities of the indicated HCC cell lines were evaluated by transwell assays. (J-N) In vivo metastatic experiments revealed that TLR4 and PTK2 upregulation was essential for KLF7-fostered HCC metastasis. (J) Representative bioluminescent pictures of liver tumors and rate of lung metastasis. (K) Bioluminescent signals of liver tumors were dynamically monitored. (L) Number of lung-colonizing nodules. (M) Typical H&E pictures of metastatic lung nodules. (N) Overall survival of different groups. *P < 0.05.