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Updated: Dec 13, 2025

Induction and Analysis of Epithelial to Mesenchymal Transition
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GINS2 promotes EMT in pancreatic cancer via specifically stimulating ERK/MAPK signaling

Longping Huang1, Si Chen2, Haijun Fan1

  • 1Department of General Surgery, Hepatobiliary Surgery, The Fourth People's Hospital of Shenyang, Shenyang, 110031, China.

Cancer Gene Therapy
|August 5, 2020
PubMed

Insights

Go-Ichi-Ni-San 2 (GINS2) oncogene overexpression drives pancreatic cancer (PC) progression by promoting epithelial-mesenchymal-transition (EMT) through the ERK/MAPK pathway. GINS2 is linked to advanced stages and poor prognosis in PC patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Go-Ichi-Ni-San 2 (GINS2) is a newly identified oncogene implicated in various cancers.
  • The specific role of GINS2 in pancreatic cancer (PC) development and progression remains largely uncharacterized.
  • Epithelial-mesenchymal-transition (EMT) is a critical process in cancer metastasis, particularly in pancreatic cancer.

Purpose of the Study:

  • To investigate the role of GINS2 in epithelial-mesenchymal-transition (EMT)-stimulated pancreatic cancer (PC).
  • To explore the association between GINS2 expression and clinicopathological features and prognosis in PC patients.
  • To elucidate the underlying molecular mechanisms, including the involvement of the ERK/MAPK signaling pathway.

Main Methods:

  • Analysis of GINS2 expression in human PC specimens and correlation with clinicopathological parameters and survival.
  • In vitro studies using PC cell lines to assess the effects of GINS2 overexpression or silencing on EMT, cell motility, and signaling pathways.
  • In vivo experiments to evaluate the impact of GINS2 on liver metastasis in a mouse model, with and without MEK inhibitor treatment.

Main Results:

  • GINS2 was overexpressed in PC specimens and associated with larger tumor size, advanced T stage, vascular invasion, and poorer prognosis.
  • GINS2 overexpression promoted EMT in vitro, enhancing cell motility and activating EMT and ERK/MAPK signaling pathways.
  • GINS2 silencing inhibited EMT, and its effects on EMT and metastasis in vivo were reversed by a MEK inhibitor, indicating a role in ERK/MAPK activation.

Conclusions:

  • GINS2 overexpression is a significant factor in pancreatic cancer progression, correlating with advanced clinical stages and poor patient survival.
  • GINS2 promotes EMT in pancreatic cancer through the activation of the ERK/MAPK signaling pathway, both in vitro and in vivo.
  • Targeting the GINS2-ERK/MAPK axis may represent a potential therapeutic strategy for pancreatic cancer.

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