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

Figure 7 Y-box binding protein 1 suppresses the function of sorafenib in the PI3K/Akt signaling pathway, and blockade of the PI3K/Akt signaling pathway inhibits the promoting effect of YB-1 on proliferation. A-D: The protein expression levels of phosphorylated protein kinase B (p-Akt), protein kinase B (Akt), phosphoinositide-3-kinase (PI3K), and phosphorylated PI3K (p-PI3K) were detected by Western blot analysis in cells infected with lentivirus vector as a negative control (Lv-NC)±sorafenib vs cells infected with lentivirus encoding Y-box protein 1 (Lv-YB-1) ± sorafenib groups and lentivirus encoding non-specific short hairpin RNA as a negative control (Lv-shNC)±sorafenib vs cells infected with lentivirus encoding short hairpin RNA targeting Y-box binding protein 1 (Lv-shYB-1) ± sorafenib groups of HepG2 (A, B) and Huh7 (C, D) cells; E-H: Western blot analysis was also applied to evaluate the expression of p-Akt, Akt, p-PI3K and PI3K in the Lv-NC + sorafenib, Lv-NC + LY294002 + sorafenib, Lv-YB-1 + sorafenib, Lv-YB-1 + LY294002 + sorafenib groups of HepG2 (E, G) and Huh7 (F, H) cells. Protein samples derived from the same experiment and gels were processed in parallel; I, J: Flow cytometry was conducted to analyze the cell cycle distribution; K-M: Western blot analysis showed proliferating cell nuclear antigen (PCNA) protein expression, and its protein levels were measured by scanning densitometry. ^aP < 0.05, ^bP < 0.01, ^cP < 0.001 vs the indicated groups.