Abstract

BackgroundThis study aims to analyse the expression of human MOF in endometrial carcinoma cells and its relationship with estrogen and estrogen receptor and to investigate the effect of estrogen–human MOF on the malignant biological behaviours of endometrial carcinoma cells.MethodsThe expression of human MOF was detected in different endometrial tissues by immunohistochemistry. The effects of human MOF, human MOF combined with estrogen stimulation and estrogen plus anti-human MOF antibody blocking on the proliferation of endometrial carcinoma cells were evaluated by western blotting, real-time polymerase chain reaction, cell proliferation assay and cell cycle distribution. Bioinformatics was used to identify the correlations of human MOF and estrogen and involved pathways.ResultsThe expression levels of human MOF in endometrial carcinoma tissues were significantly higher than that in atypical hyperplasia and normal endometrial tissues. High expression of human MOF was associated with late-stage cancer, lymph node metastasis and short survival time, and it was also an independent prognostic risk factor for endometrial carcinoma. After human MOF knockdown, the proliferation, migration and invasive capacity of Ishikawa cells decreased and cell apoptosis increased. After stimulation with estrogen, the PI3K/Akt and Ras–Raf–MEK–ERK signalling pathways were activated, and the expression of the human MOF protein was increased. human MOF (KAT8) expression showed a positive correlation with ESR1 expression, and KAT8-associated genes were enriched in the cell cycle pathways and splicing pathways.ConclusionHuman MOF was highly expressed in endometrial carcinoma and associated with proliferation. Estrogen/estrogen receptor enhanced human MOF expression; promoted the proliferation, migration and invasion of Ishikawa cells; and inhibited cell apoptosis by activating the PI3K/Akt and Ras–Raf–MEK–ERK signalling pathways.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.