Journal: Frontiers in Oncology

Article Title: Crosstalk between protein kinases AKT and ERK1/2 in human lung tumor-derived cell models

doi: 10.3389/fonc.2022.1045521

Figure Lengend Snippet: Dependence of the interplay between ERK and AKT signaling pathways on extracellular contacts. (A) Focal adhesion kinase inhibitor PF573228 (+Fi; 10 µM) attenuates the MEK kinase inhibitor selumetinib-induced increase of AKT phosphorylation in control and cisplatin-treated lung cancer-derived cells, except A549 cells. (B) PF573228 prevents the AKT inhibitor capivasertib-induced increase in ERK phosphorylation in control and cisplatin-treated lung cancer-derived cells. (C) Cells grown in suspension (Susp) under agitation, in contrast to adherent cells (Adh), do not show alternative kinase activation after the treatment with inhibitors. Representative Western blots are shown. Coomassie-stained protein gels are presented as loading controls. 6-hour-long exposures to the drugs were used. DM – vehicle control (DMSO), SEL – selumetinib (10 µM), +cis – cisplatin (90 µM), CAP – capivasertib (10 µM), AKTi – AKT inhibitor VIII (10 µM).

Article Snippet: The following inhibitors of ERK and AKT signal pathways were used in this study: PI3K inhibitor idelalisib CAL-101 (10 µM; Cayman Chemical, Ann Arbor, MI, USA); Akt inhibitor VIII (10 µM, Merck) and capivasertib AZD5363 (10 µM, Cayman chemical); MEK1/2 inhibitors selumetinib AZD6244 (10 µM, Selleck Chemicals, Houston, TX, USA), trametinib (1 µM, Cayman chemical); ERK inhibitor SCH772984 (1 µM, Cayman chemical); FAK inhibitor PF573228 (10 µM, Merck.).

Techniques: Derivative Assay, Activation Assay, Western Blot, Staining