Research Paper Volume 14, Issue 22 pp 9000—9019

NAP1L5 targeting combined with MYH9 Inhibit HCC progression through PI3K/AKT/mTOR signaling pathway

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Figure 6. NAP1L5 regulates the PI3K/AKT/MTOR signaling pathway in hepatoma cells. (A) Venn diagram of the mass spectrometry analysis of MHCC97H cells overexpressing NAP1L5 and transferred into the control vector. (B) Mass spectrometry analysis of the GO functional enrichment map of MHCC97H cells overexpressing NAP1L5. (C) Enrichment of differentially expressed gene pathways in NAP1L5-overexpressing and MHCC97H cells transfected with the control vector. (D) Western blotting was used to detect the expression of p-AKT and p-mTOR in HepG2 and MHCC97H cells overexpressing NAP1L5. (E) Western blotting was used to detect the expression of p-AKT and p-mTOR in HepG2 and MHCC97H cells downregulated by NAP1L5. (F) Western blotting was used to analyze the expression of key molecules involved in cell cycle regulation, EMT and apoptosis in HepG2 and MHCC97H cells overexpressing NAP1L5. (G) Western blotting was used to analyze the expression of key molecules involved in cell cycle regulation, EMT and apoptosis in HepG2 and MHCC97H cells downregulated by NAP1L5.