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. 2017 Sep 16;8(58):98068–98083. doi: 10.18632/oncotarget.20956

Figure 3. PTEN and LKB1 synergistically enhance the activation of the AKT/mTOR pathway and promote the proliferation of pNET cell lines.

Figure 3

(A) The cell proliferative rates of QGP-1 cells without (QGP-1/shLuc) or with knockdown of PTEN (QGP-1/shPTEN), LKB1 (QGP-1/shLKB1) and both PTEN and LKB1 (QGP-1/shPTEN/LKB1). *, QGP-1/shLuc vs. QGP-1/shPTEN/LKB1, P < 0.01 (B) The cell proliferative rates of NIT-1 cells without (NIT-1/shLuc) or with knockdown of PTEN (NIT-1/shPTEN), LKB1 (QGP-1/shLKB1) and both PTEN and LKB1 (QGP-1/shPTEN/LKB1). *, NIT-1/shLuc vs. NIT-1/shPTEN/LKB1, P = 0.01 (C) The phosphorylated protein expression of AKT, mTOR, S6K and 4EBP1 as well as the protein expression of c-Myc, PTEN and LKB1 in QGP-1 and NIT-1 cells without or with knockdown of PTEN, LKB1 and both PTEN and LKB1 by western blot. Actin was used as the internal control.