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Original Research

Open Access

GINS2 regulates epithelial mesenchymal transformation and cell cycle in endometrial carcinoma by stimulating ERK/MAPK signaling

  • Min Zhou1,*,
  • Wei Hua1
  • Yulan Sun1

1Department of Pathology, The First Affiliated Hospital of Harbin Medical University, 150001 Harbin, Heilongjiang, China

DOI: 10.22514/ejgo.2023.067 Vol.44,Issue 4,August 2023 pp.156-163

Submitted: 07 June 2023 Accepted: 07 July 2023

Published: 15 August 2023

*Corresponding Author(s): Min Zhou E-mail: zhoumin_668@163.com

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.


Keywords

Endometrial cancer (EC); GINS2; Cell cycle; EMT; ERK/MAPK pathway


Cite and Share

Min Zhou,Wei Hua,Yulan Sun. GINS2 regulates epithelial mesenchymal transformation and cell cycle in endometrial carcinoma by stimulating ERK/MAPK signaling. European Journal of Gynaecological Oncology. 2023. 44(4);156-163.

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