Publication: Elp3 activates the JNK/MAPK pathway through histone acetylation to promote gastric cancer proliferation, migration, and invasion
Authors
Hao Shang ; Xiali Shi ; Hanmei Jiang ; Ji Di
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Publisher
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Universidad de Murcia, Departamento de Biologia Celular e Histiologia
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DOI
https://doi.org/10.14670/HH-25-001
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info:eu-repo/semantics/article
Description
Abstract
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.
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