Additional file 4: of AKT1 restricts the invasive capacity of head and neck carcinoma cells harboring a constitutively active PI3 kinase activity

CAL33-shControl cells untreated or treated with MK-2206 and CAL33-shAKT1.1 and 1.2 cells electrical resistance measurements. Raw output file of the ECIS measurement of resistance in MΩ at a frequency of 4000 Hz. (XLS 220 kb

Additional file 8: of AKT1 restricts the invasive capacity of head and neck carcinoma cells harboring a constitutively active PI3 kinase activity

Detroit562 cells untreated or treated with MK-2206 or Rapamycin electrical resistance measurements. Raw output file of the ECIS measurement of resistance in MΩ at a frequency of 4000 Hz. (XLS 213 kb

Additional file 13: of AKT1 restricts the invasive capacity of head and neck carcinoma cells harboring a constitutively active PI3 kinase activity

Figure S4 Analysis of e-cadherin expression and localization by immunofluorescence in CAL27 and Detroit562 cells. Immunostaining of e-cadherin (green) and Alexa555-phalloidin (red) staining of the actin cytoskeleton (F-actin) in CAL27 and Detroit562 cells treated with the pan-AKT inhibitor MK-2206 (MK), Rapamycin (Rapa) or Erlotinib (Erlo). Nuclear DNA was counterstained with Hoechst 33,342 (blue). (PDF 247 kb

Additional file 1: of AKT1 restricts the invasive capacity of head and neck carcinoma cells harboring a constitutively active PI3 kinase activity

CAL33-shControl cells treated with Erlotinib, Rapamycin and MK-2206 electrical resistance measurements. Raw output file of the ECIS measurement of resistance in MΩ at a frequency of 4000 Hz. (XLS 432 kb

Additional file 9: of AKT1 restricts the invasive capacity of head and neck carcinoma cells harboring a constitutively active PI3 kinase activity

Electrical data used to generate the figures. The ECIS measurements of resistance in MΩ at a frequency of 4000 Hz were normalized to the first measurement and plotted in the Graphpad Prism software to generate the traces shown in Figs. 3a-c and 4a. The quantification data were obtained by measuring the mean resistance increase during the cell attachment phase (from 4 to 8 h after cell spreading). (XLSX 140 kb

Additional file 5: of AKT1 restricts the invasive capacity of head and neck carcinoma cells harboring a constitutively active PI3 kinase activity

CAL33-shControl cells untreated or treated with MK-2206 and CAL33-shAKT1.1 and 1.2 cells electrical resistance measurements. Raw output file of the ECIS measurement of resistance in MΩ at a frequency of 4000 Hz. (XLS 86 kb

Additional file 2: of AKT1 restricts the invasive capacity of head and neck carcinoma cells harboring a constitutively active PI3 kinase activity

CAL33-shControl cells untreated or treated with Rapamycin and MK-2206 electrical resistance measurements. Raw output file of the ECIS measurement of resistance in MΩ at a frequency of 4000 Hz. (XLS 213 kb

Additional file 10: of AKT1 restricts the invasive capacity of head and neck carcinoma cells harboring a constitutively active PI3 kinase activity

Figure S1. AKT1 and AKT2 isoform expression in CAL33, Detroit562 and CAL27 cells. AKT1 and AKT2 expression levels were evaluated by immunoblot with specific anti-AKT antibody in CAL33 cells expressing a control shRNA (shCont), two independent shRNA sequences targeting AKT1 (sh1.1 and sh1.2) and in Detroit562 and CAL27 cells. GAPDH was used as a loading control. (PDF 26 kb

Additional file 3: of AKT1 restricts the invasive capacity of head and neck carcinoma cells harboring a constitutively active PI3 kinase activity

CAL33-shControl cells untreated or treated with MK-2206 and CAL33-shAKT1.1 and 1.2 cells electrical resistance measurements. Raw output file of the ECIS measurement of resistance in MΩ at a frequency of 4000 Hz. (XLS 147 kb