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Fig. 2 | Journal of Experimental & Clinical Cancer Research

Fig. 2

From: Targeted inhibition of PDGFRA with avapritinib, markedly enhances lenvatinib efficacy in hepatocellular carcinoma in vitro and in vivo: clinical implications

Fig. 2

Lenvatinib resistance in HCC cells is acquired via PDGFRA overexpression. (A) qPCR was used to detect the mRNA levels of PDGFR in the SMMC-7721-PT, SMMC-7721-LR, SNU-449-PT and SNU-449-LR cells. (B) Western blot analysis was conducted to assess the protein expression levels of PDGFRA in the four cell lines. (C) Western blot analysis of PDGFRA protein levels in the different HCC cell lines. (D) The colony formation capacity of PDGFRA-overexpressing and control SNU-449 and SMMC-7721 cells was assessed by a clonogenic assay following lenvatinib treatment. (E) SMMC-7721/SNU-449 cells overexpressing PDGFRA and control cells were treated with lenvatinib, and their cell survival curves were depicted. (F) PDGFRA was knocked down in Huh7, SNU-398, SMMC-7721-LR, and SNU-449-LR cells, and cell survival was assessed after treatment with various concentrations of lenvatinib. (G) Representative xenograft tumors and tumor growth curves for the following three groups at the endpoint in a subcutaneous implantation mouse model: SMMC-7721-PT group, SMMC-7721-PT plus lenvatinib group, and SMMC-7721-LR plus lenvatinib group (N = 5 for each group). (H) Western blot analysis was used to determine the levels of PDGFRA protein in the subcutaneous tumors from different groups. (I) Representative H&E staining and IHC images of PDGFRA in the subcutaneous implantation mouse model

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