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Oncogenic function of TRIM2 in pancreatic cancer by activating ROS-related NRF2/ITGB7/FAK axis

Qiqing Sun1,2,3,4, Zeng Ye1,2,3,4, Yi Qin1,2,3,4

  • 1Department of Pancreatic Surgery, Fudan University Shanghai Cancer Center, 200032, Shanghai, China.

Oncogene
|September 15, 2020
PubMed

Insights

High tripartite motif-containing 2 (TRIM2) expression in pancreatic cancer predicts poor survival. TRIM2 promotes tumor growth and spread by activating the ROS-related NRF2/ITGB7/FAK pathway.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Tripartite motif-containing 2 (TRIM2) is implicated in various cancers.
  • Its role in pancreatic cancer remains largely unexplored.
  • Understanding TRIM2's function is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the expression patterns and functional significance of TRIM2 in pancreatic cancer.
  • To elucidate the underlying molecular mechanisms by which TRIM2 influences pancreatic cancer progression.

Main Methods:

  • Analysis of TRIM2 expression in pancreatic tumor samples.
  • In vitro and in vivo functional assays following TRIM2 silencing.
  • Investigation of TRIM2's impact on ROS-related NRF2/ARE and integrin/FAK signaling pathways.

Main Results:

  • TRIM2 is highly expressed in pancreatic tumors and correlates with poor patient outcomes.
  • TRIM2 silencing inhibits pancreatic cancer cell proliferation, migration, invasion, and tumorigenicity.
  • TRIM2 activates the ROS-related NRF2/ITGB7/FAK axis, promoting cancer progression.

Conclusions:

  • Upregulated TRIM2 is a prognostic marker for pancreatic cancer patients.
  • TRIM2 drives pancreatic cancer progression through the ROS-related NRF2/ITGB7/FAK signaling axis.
  • Targeting TRIM2 may offer a novel therapeutic strategy for pancreatic cancer.

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