Journal
TRANSLATIONAL ONCOLOGY
Volume 15, Issue 1, Pages -Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.tranon.2021.101299
Keywords
EIF1A; Pituitary adenoma; Cell proliferation; Cell migration; MAPK
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This study found that EIF1A is upregulated in human pituitary adenoma cells and depletion of EIF1A can severely limit cell proliferation, weaken cell migration capacity, and increase apoptosis of tumor cells. The study demonstrates that EIF1A plays a prominent role in facilitating tumor cell proliferation and migration.
EIF1A encodes a translation initiation factor in eukaryocyte and aberrant expression of EIF1A is deemed to be associated with dysfunctions in intracranial diseases. The goal of this research was to explore the impacts of EIF1A on progression of human pituitary adenoma (PA). We employed immunohistochemistry to assess the expression of EIF1A in PA and para-carcinoma tissues. After constructing EIF1A-knockdown cell models via lentivirus infection, we examined cell proliferation through CCK-8 assay and Celigo cell counting assay. Flow cytometry was utilized to detect cell apoptosis and the migration ability of experimental cells was estimated using wound-healing assay and Transwell assay. The activity of the apoptosis-related factor, Caspase 3, was also examined via Caspase 3 activity assay. Lastly, in vivo xenograft mouse models were established to verify findings derived from in vitro cell models. Our results affirmed upregulation of EIF1A in PA cells and revealed that depletion of EIF1A could seriously limit cell proliferation and weaken the capacity of cell migration, and also enhance apoptosis of tumor cells. Mechanistically, degradation in cell growth mediated by EIF1A knockdown may involve in activation of MAPK signaling but inactivation of PI3K/AKT signaling pathway. This study indicates EIF1A plays a prominent role in facilitating tumor cell proliferation and migration which may further contribute to PA progression.
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