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Development of a Genetically Engineered Mouse Model Recapitulating LKB1 and PTEN Deficiency in Gastric Cancer

Kuan-Te Fang1, Hsin Hung1, Nga Yin Sadonna Lau1,2

  • 1Institute of Biomedical Sciences, National Sun Yat-Sen University, Kaohsiung 80424, Taiwan.

Cancers
|December 23, 2023
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Summary

Deleting LKB1 and PTEN genes in stomach cells promotes gastric cancer (G.C.) development. This creates a tumor microenvironment supporting G.C. cell proliferation, angiogenesis, and metastasis.

Keywords:
E-cadheringastric cancerintestinal type of gastric cancerliver kinase B1mouse models of cancerphosphatase and tensin homologphosphoinositide 3-kinase signaling pathway

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • LKB1 and PTEN are crucial tumor suppressor genes involved in gastric cancer (G.C.) development.
  • LKB1 regulates cellular metabolism and epithelial junction stability via AMPK and E-cadherin.
  • PTEN negatively regulates the PI3K signaling pathway, a common mutation target in cancers.

Purpose of the Study:

  • To investigate the role of LKB1 and PTEN in gastric cancer development using a targeted genetic approach.
  • To elucidate how the loss of LKB1 and PTEN function in stomach cells contributes to G.C. tumorigenesis.
  • To analyze the impact of these genetic alterations on tumor histopathology, invasiveness, metastasis, angiogenesis, and the tumor microenvironment.

Main Methods:

  • Utilized the H+/K+ ATPase Cre transgene strain for cell-specific Cre recombinase expression in stomach parietal cells.
  • Achieved conditional deletion of LKB1 and PTEN genes specifically within the stomach.
  • Monitored the development of G.C. and analyzed tumor characteristics, including histopathology, angiogenesis, and microenvironment changes.

Main Results:

  • Conditional deletion of PTEN and LKB1 in the stomach successfully induced G.C. development.
  • The loss of these tumor suppressors created a pro-tumorigenic microenvironment.
  • This environment was characterized by increased cancer cell proliferation, enhanced angiogenesis, and promoted metastasis.

Conclusions:

  • Simultaneous loss of LKB1 and PTEN function is sufficient to drive gastric cancer initiation and progression.
  • The resulting tumor microenvironment significantly supports G.C. tumorigenesis through proliferation, angiogenesis, and metastasis.
  • Targeted deletion of these genes provides a valuable model for studying human gastric adenocarcinoma.