Fig. 5: EIF3B modulates ERK phosphorylation in LSCC cells via the kinase activity of MAP2K2. | Cell Death Discovery

Fig. 5: EIF3B modulates ERK phosphorylation in LSCC cells via the kinase activity of MAP2K2.

From: EIF3B stabilizes MAP2K2 to activate the ERK pathway and promote the progression of laryngeal squamous cell carcinoma

Fig. 5

A Cell lysates were collected at 6, 12, 24, and 48 h in AMC-HN-8 and TU212 cells that induced EIF3B overexpression and control. The total levels and phosphorylation levels of MAP2K2 and ERK were detected by WB. B The total levels and phosphorylation levels of ERK were detected by WB in AMC-HN-8 and Tu212 cells with EIF3B overexpression or MAP2K2 knockdown. C Wild-type MAP2K2 (WT) or kinase death mutant (K101A) was re-expressed in MAP2K2 knockdown and control AMC-HN-8 and TU212 cells. The total level and phosphorylation level of ERK were detected by WB. D Purify MAP2K2 (WT or K101A) and ERK proteins. In the presence of ATP, MAP2K2 and ERK were incubated, and total level and phosphorylation level of ERK were detected by WB. E The cells AMC-HN-8 and TU212 with EIF3B overexpression and control were pretreated with the MEK inhibitor U0126 (10 μM) for 1 h, and total level and phosphorylation level of ERK were detected. The proliferation (F) and clonal formation (G) of EIF3B overexpressed AMC-HN-8 and Tu212 cells were examined by MAPK/ERK signaling pathway inhibitor (U0126). The representative images were selected from at least 3 independent experiments. The data were presented as the mean ± SD (n = 3). **P < 0.01, ***P < 0.001.

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