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. 2020 Sep 30;13:9701–9719. doi: 10.2147/OTT.S256378

Figure 7.

Figure 7

Silencing ITM2B was significantly active PI3K/Akt signaling pathway in lung cancer cells. (A) Hierarchical clustering and heatmap analysis of RNA sequencing results of ITM2B knockdown LTEP-a-2 cells and control group; (B) Pathway analysis of the differentially expressed genes using the KEGG database; (C and D) The phosphorylation and total expression levels of PI3K and Akt in LTEP-a-2 cells (C) and SPC-A-1 cells (D). Cells infected with SH-ITM2B lentivirus and/or Deguelin. The expression levels of the phosphorylated proteins were normalized to those of the respective total protein; (E) Proliferation rate of LTEP-a-2 cells was analyzed using CCK-8 assays every 24 hours following treatment with SH-ITM2B lentivirus and/or Deguelin treatment compared with the control group; (F) Ki67 levels of LTEP-a-2 cells were analyzed using RT-qPCR following SH-ITM2B lentivirus and/or Deguelin treatment compared with the control group; (G) Tumor growth rate of lung cancer xenograft with SH-ITM2B lentivirus and/or Deguelin treatment compared with the control group; (H) Kaplan–Meier overall survival curve in mice with SH-ITM2B lentivirus and/or Deguelin treated compared with the control group. Mean±SEM, *P<0.05, **P<0.01, ***P<0.005, ****P<0.001.