Abstract
Endometrial cancer (EC) is one of the three main gynecological cancers. Identifying new therapeutic targets and further elucidating the molecular mechanisms of EC tumorigenesis have important implications for women’s health. The Go-Ichi-Ni-San (GINS) family, which includes four subunits (GINS1–4), has specific functions in DNA replication and cell cycle. The Cancer Genome Atlas (TCGA) data showed that GINS2 transcription level is upregulated in endometrial cancer tissue. However, the possible role of GINS2 in EC progression is still unknown. Herein, we explored the role of GINS2 in EC. We noticed that GINS2 was overexpressed in EC cells. GINS2 knockdown suppressed the proliferation of EC cells and induced cell cycle arrest. We further noticed that GINS2 knockdown restrained the Epithelial mesenchymal transformation (EMT) of EC cells. Mechanically, its downregulation suppressed the extracellular regulated protein kinase (ERK)/Microtubule-Associated Protein Kinase (MAPK) pathway, thereby suppressing EC progression. Thus, GINS2 has the potential to act as a therapeutic target for EC.
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