EIF5B/mitogen-activated protein kinase 1 axis drives tumor progression and confers dual resistance to chemotherapy and immunotherapy in colonic adenocarcinoma

Figure 4 Eukaryotic translation initiation factor 5B depends on the mitogen-activated protein kinase 1 signaling pathway to enhance colonic adenocarcinoma cell proliferation, migration, and invasion. A: Kyoto Encyclopedia of Genes and Genomes enrichment analysis of eukaryotic translation initiation factor 5B (EIF5B) using three independent datasets; B-E: Western blotting was used to investigate the effects of EIF5B overexpression and knockdown on mitogen-activated protein kinase 1 (MAPK1) and phosphorylated MAPK1 expression; F-I: Evaluation of proliferation, migration and invasion in colonic adenocarcinoma (COAD) cells treated as follows: Lentivirus negative control + dimethyl sulfoxide (DMSO), lentivirus expressing EIF5B (LV-EIF5B) + DMSO, and LV-EIF5B + MAPK1 inhibitor SCH772984; J-M: Evaluation of proliferation, migration and invasion in COAD cells treated as follows: Short hairpin RNA negative control + DMSO, short hairpin RNA targeting EIF5B (sh-EIF5B) + DMSO, and sh-EIF5B + MAPK1 activator tert-butylhydroquinone. All photomicrographs were captured at × 200 magnification. n = 3 independent experiments, with values expressed as the mean ± SD. Group comparisons were conducted as follows: Independent-samples t-tests or non-parametric tests for two groups, one-way analysis of variance (ANOVA) or non-parametric tests for single-factor multi-group comparisons and two-way ANOVA for experiments with two independent factors. ^aP < 0.05. ^bP < 0.01. ^cP < 0.001. ^dP < 0.0001. HIV: Human immunodeficiency virus; LV-NC: Lentivirus negative control; MAPK1: Phosphorylated mitogen-activated protein kinase; OD: Optical density; sh-NC: Short hairpin RNA negative control; TCGA: The Cancer Genome Atlas.