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Stefan Thiem1, Thomas P Pierce, Michelle Palmieri

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Chronic inflammation drives gastrointestinal cancers via GP130 signaling. Targeting the PI3K/mTORC1 pathway, not STAT3, with RAD001 effectively inhibited tumor growth in preclinical models.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Gastroenterology

Background:

  • Gastrointestinal cancers often involve chronic inflammation and IL-6 cytokine family signaling, activating the GP130/JAK/STAT3 pathway.
  • STAT3 is crucial for tumor progression, but it's a difficult therapeutic target due to limited approved inhibitors.

Purpose of the Study:

  • To investigate the role of mTOR complex 1 (mTORC1) activation in inflammation-associated gastrointestinal tumorigenesis.
  • To determine if mTORC1 inhibition could prevent tumor initiation and progression.

Main Methods:

  • Analysis of human intestinal-type gastric cancers (IGCs) for mTORC1 and STAT3 activation.
  • Utilized a preclinical mouse model of IGC and colitis-associated colon cancer.
  • Administered the mTORC1-specific inhibitor RAD001 and assessed its effects on tumor growth, vascularization, and cell proliferation, independent of STAT3 activity.

Main Results:

  • Found parallel activation of mTORC1 and STAT3 in human IGCs.
  • GP130 ligand simultaneously activated mTORC1/S6K and STAT3 signaling in a mouse IGC model.
  • RAD001 significantly suppressed tumor initiation and progression in both murine IGC and colitis-associated colon cancer models.
  • Therapeutic effects of RAD001 were linked to reduced tumor vascularization and proliferation, independent of STAT3.
  • Discovered that GP130-mediated mTORC1 activation requires JAK and PI3K activity, but not GP130 tyrosine phosphorylation or STAT3.

Conclusions:

  • GP130-dependent activation of the PI3K/mTORC1 pathway is essential for inflammation-associated gastrointestinal tumorigenesis.
  • The mTORC1 pathway is a druggable target for treating these malignancies.
  • Clinical application of PI3K/mTORC1 inhibitors is recommended for relevant human cancers.