Abstract:
:The precise mechanism through which the two estrogen receptor subtypes, ERα and ERβ, are linked to endometrial malignant progression is not fully understood. The aim of the present study was to examine their role in endometrial carcinoma cell migration, invasion and proliferation. We also explored the correlation between the ERs and phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) pathways in endometrial carcinoma cells. Using Ishikawa and KLE cells as model systems, we performed transient transfection to upregulate ERα and ERβ expression; fluorescence microscopy analysis was then employed to evaluate transfection efficiencies, RT-PCR and western blot assays were used to evaluate the mRNA and protein levels. We further examined the effects on cell migration, invasion and proliferation. We showed that ERα raised the phosphorylation levels of PI3K p85α, activated the phosphorylation of AKT and mTOR in Ishikawa and KLE cells, but ERβ had no effect on PI3K p85α phosphorylation. Moreover, the overexpression of ERs enhanced cell migration, invasion and proliferation. The effect on the activation of the PI3K/AKT/mTOR transduction cascade by ERα explains, at least in part, the enhancement on cell invasion and proliferation exerted by overexpression of ERα. This crosstalk could be taken into account in developing novel therapeutic methods by targeting the ERα and PI3K/AKT/mTOR pathways in endometrial carcinoma.
journal_name
Oncol Repjournal_title
Oncology reportsauthors
Hou X,Zhao M,Wang T,Zhang Gdoi
10.3892/or.2013.2944subject
Has Abstractpub_date
2014-03-01 00:00:00pages
1175-82issue
3eissn
1021-335Xissn
1791-2431journal_volume
31pub_type
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