Browsing by Subject "JNK/MAPK pathway"

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    Elp3 activates the JNK/MAPK pathway through histone acetylation to promote gastric cancer proliferation, migration, and invasion
    (2026) Hao Shang; Xiali Shi; Hanmei Jiang; Ji Di; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e Histiologia
    Background. Gastric cancer (GC) seriously affects the life and health of patients, and the role of Elp3 in GC is still unclear; therefore, the aim of this study was to investigate the role and mechanism of Elp3 overexpression in GC. Methods. Elp3-overexpressing HGC27 cells were constructed with an overexpression plasmid, and Elp3 overexpressing GC nude mice were prepared, which were intervened by histone acetylation inhibitor (SAHA) or JNK pathway inhibitor (SP600125). The protein interactions between Elp3 and JNK1 were verified by Co-immunoprecipitation (Co-IP) assay. Cell prolifera tion, migration, invasion, JNK/MAPK pathway, and histopathological changes were evaluated with CCK-8, clone formation assay, scratch assay, Transwell, qRT PCR, western blot, and HE staining. Results. Elp3 interacted with JNK1 protein, and Elp3 overexpression promoted GC proliferation, invasion, migration, elevated HAT activity, and activation of the JNK/MAPK pathway. A histone acetylation inhibitor attenuated the promotional effect of Elp3 overexpression on GC and activation of the JNK/MAPK pathway. Further, inhibition of the JNK/MAPK pathway also suppressed the promotion of GC by Elp3 overexpression. Conclusion. Elp3 may be involved in GC progression by activating the JNK/MAPK pathway through histone acetylation.