Effect and mechanism of TRIP13 on promoting proliferation,migration and invasion in endometrial carcinoma
Objective:To investigate the effect of thyroid hormone receptor interactor 13(TRIP13)on the proliferation,migration and invasion of Endometrial Carcinoma(EC)and its regulatory mechanism.Methods:The expression pattern of TRIP13 in endometrial cancer were analyzed.The modulation of TRIP13 expression in endometrial cancer cells was achieved through lentiviral knockout and plasmid overexpression.CCK-8 assays,Transwell migration,and invasion experiments were conducted to assess the influence of TRIP13 on the proliferation,migration,and invasion of endometrial cancer cells.Western blot analysis was employed to evaluate the impact of TRIP13 expression on proteins in the PI3K/Akt signaling pathway.Results:Analysis of the TCGA database revealed a significantly higher expression level of TRIP13 in endometrial cancer tissues compared to normal endometrial tissues(P<0.05).High TRIP13 expression was significantly and positively associated with a lower survival rate among patients with endometrial cancer(P<0.001).Elevated TRIP13 expression was found to accelerate the proliferation,migration,and invasion of endometrial cancer cells(P<0.01)and was linked to a significant upregulation in the expression of p-PI3K and p-Akt(P<0.05).Conversely,downregulating TRIP13 reversed these outcomes.Conclusion:TRIP13 regulates the PI3K/Akt signaling pathway to facilitate the proliferation,migration and invasion of endometrial cancer.
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