Figure 7.

PD amplifies the anticancer effects of sorafenib on HCC in vitro and in vivo

(A) The concentration of sorafenib in lysosomes with or without PD treatment (3 μM) was analyzed by LC-MS/MS, showing that PD induced sorafenib release from lysosomes. (B–D) HCC cells were treated with PD (1.5 μM) in the presence or absence of sorafenib (10 μM) as indicated. Then, caspase 3/7 activity was measured by flow cytometry (B), cell viability was tested by WST-1 assay (C), and the cell growth was determined by colony formation assay (D). (E) The therapeutic response of PD and sorafenib combined treatment on the HCC MiniPDX model. The relative proliferation rate of the HCC MiniPDX model upon treatment with PD (i.g. 4 mg/kg) and sorafenib (i.g. 10 mg/kg) was measured (n = 6). (F–J) Nude mice bearing HepG2-derived xenografts received PD (4 mg/kg), sorafenib (10 mg/kg), or vehicle control by oral gavage every 3 days, respectively (n = 6) (F). The tumor photos (G), tumor volume curves (H), tumor weights (I), and IHC staining for Ki-67, CD31, p-ERK, and Gal3/DAPI in the indicated tumor xenografts (J) are shown. All data are presented as the mean ± SD; ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001; ns, no significance.