KLF2 transcription suppresses endometrial cancer cell proliferation, invasion, and migration through the inhibition of NPM1

Endometrial cancer (EC) is the most common gynaecologic malignancy. This study was to explore the role of kruppel-like factor 2 (KLF2) in EC cell behaviours. The expression of KLF2 in EC and its correlation with NPM1 were first predicted on the database. Levels of KLF2 and nucleophosmin 1 (NPM1) in EC cell lines were then determined. After transfection of the overexpression vector of KLF2 or NPM1, cell proliferation, invasion, and migration were evaluated. The binding relationship between KLF2 and the NPM1 promoter was analysed. KLF2 was downregulated while NPM1 was upregulated in EC cells. KLF2 overexpression reduced the proliferation potential of EC cells and the number of invaded and migrated cells. KLF2 was enriched in the NPM1 promoter and inhibited NPM1 transcriptional level. NPM1 overexpression neutralised the effects of KLF2 overexpression on suppressing EC cell growth. Collectively, KLF2 was decreased in EC cells and KLF2 overexpression increased the binding to the NPM1 promoter to inhibit NPM1 transcription, thus suppressing EC cell growth. <b>What is already known on this subject?</b> Endometrial cancer (EC) sees a significant increase in prevalence globally with poor survival rates. KLF2 has been recognised as a tumour suppressor in a variety of malignancies. NPM1 can regulate EC cell viability and apoptosis.<b>What do the results of this study add?</b> This study highlighted that KLF2 produces an anti-tumour effect in EC and KLF2 can regulate NPM1 expression in EC and thereafter affect the proliferative, migratory, and invasive abilities of EC cells.<b>What are the implications of these findings for clinical practice and/or further research?</b> KLF2 overexpression suppresses NPM1 transcription and inhibits EC cell growth. Targeting KLF2 overexpression may be useful for EC treatment in clinical practice. <b>What is already known on this subject?</b> Endometrial cancer (EC) sees a significant increase in prevalence globally with poor survival rates. KLF2 has been recognised as a tumour suppressor in a variety of malignancies. NPM1 can regulate EC cell viability and apoptosis. <b>What do the results of this study add?</b> This study highlighted that KLF2 produces an anti-tumour effect in EC and KLF2 can regulate NPM1 expression in EC and thereafter affect the proliferative, migratory, and invasive abilities of EC cells. <b>What are the implications of these findings for clinical practice and/or further research?</b> KLF2 overexpression suppresses NPM1 transcription and inhibits EC cell growth. Targeting KLF2 overexpression may be useful for EC treatment in clinical practice.