All-Trans Retinoic Acid Induces Proliferation, Survival, and Migration in A549 Lung Cancer Cells by Activating the ERK Signaling Pathway through a Transcription-Independent Mechanism

Figure 2

Effect of AGN193109 and Ro 41-5253 inhibitors on ATRA-induced ERK activation. A549 cells were serum-starved for 18 h, treated or nontreated (NT) with 5 μM of ATRA for 15 minutes. Cells were preincubated for 1 h with 10 μM of AGN193109 or 20 μM of Ro 41-5253 alone or in combination with ATRA. The phosphorylated form of ERK was detected by western blot using specific antibodies. β-Actin was used as the loading control. The graph represents the densitometric values of ERK phosphorylation in three independent experiments (means ± SEM, ; compared with NT cells, analysis of variance and Newman-Keuls test).