Fig. 6

Alteration of cellular bioactivies with the changes of rpS6 phosphorylation from Akt2 interference or phosphorylation inhibition. a CCK-8 assay revealed rpS6 hyphosphorylation from Akt2 overexpressing in HBE greatly promoted cells proliferation (left; P < 0.05), and p-rpS6 reducing in H1650 and SK-MES-1 cells from Akt2 knockdown or phosphorylation inhibition markedly deteriorated cells proliferation (middle and left; P < 0.05). b Influence of p-rpS6 on cell cycles in HBE and NSCLC cell lines (P < 0.05). c Wound-healing assay was performed after rpS6 hyphosphorylation in HBE (left; P < 0.05), and cell migration assay was carried out after p-rpS6 reduce in H1650 and SK-MES-1 cell lines (middle and left; P < 0.05). CCK-8 experiments were carried out in sextuplicate, and the remaining tests were triplicate. Data are presented as mean ± SD. oe-Akt1: overexpression of Akt1; oe-NCa1: negative control for oe-Akt1; oe-Akt2: overexpression of oe-Akt2; oe-NCa2: negative control for oe-Akt2; oe-Akt3: overexpression of oe-Akt3; oe-NCa3: negative control for oe-Akt3. sh-Akt1: knockdown for Akt1; sh-NCa1: negative control for sh-Akt1; sh-Akt2: knockdown for Akt2; sh-NCa2: negative control for sh-Akt2; sh-Akt3: knockdown for Akt3; sh-NCa3: negative control for sh-Akt3. *: vs the corresponding blank control cell lines without any transfection (HBE, H1650 and SK-MES-1 respectively), P < 0.05; #: vs the corresponding control cell lines with the negative control (NC) vectors transfection (HBE + oe-NC, H1650 + sh-NC, SK-MES-1 + sh-NC, respectively), P < 0.05