Y-box binding protein 1 augments sorafenib resistance via the PI3K/Akt signaling pathway in hepatocellular carcinoma

Figure 5 Sorafenib efficiency improves after Y-box binding protein 1 knockdown in vivo. A: The morphologies of collected tumors in subcutaneous Huh7 xenografts in nude mice; B: Tumor growth curves; C: Tumor weights were measured after collection; D: Hematoxylin-eosin (HE) and immunohistochemical staining for proliferating cell nuclear antigen; E, F: Western blot analysis showed Y-box binding protein 1 (YB-1), phosphorylated protein kinase B (p-Akt), protein kinase B (Akt), phosphorylated phosphoinositide-3-kinase (p-PI3K), and phosphoinositide-3-kinase (PI3K) expression in cells infected with lentivirus encoding non-specific short hairpin RNA as a negative control (Lv-shNC) ± sorafenib vs lentivirus containing short hairpin RNA targeting YB-1 (Lv-shYB-1) ± sorafenib groups. p-Akt (normalized to Akt) and p-PI3K (normalized to PI3K) protein levels were measured by scanning densitometry. Protein samples derived from the same experiment and gels were processed in parallel. ^aP < 0.05, ^bP < 0.01, ^cP < 0.001 vs the indicated groups. PCNA: Proliferating cell nuclear antigen.