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Cancer associated fibroblast FAK regulates malignant cell metabolism
Fevzi Demircioglu1, Jun Wang2, Juliana Candido3
1Centre for Tumour Biology, Barts Cancer Institute, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London, EC1M 6BQ, UK.
Nature Communications
|March 12, 2020
Summary
Cancer-associated fibroblasts (CAFs) regulate cancer cell metabolism via FAK signaling. Low FAK in CAFs enhances tumor growth by promoting cancer cell glycolysis, impacting patient survival.
Area of Science:
- Oncology
- Cancer Biology
- Metabolic Pathways
Background:
- Cancer-associated fibroblasts (CAFs) influence tumor progression.
- Mechanisms by which CAFs regulate cancer cell metabolism are not fully understood.
Purpose of the Study:
- To elucidate the role of Focal Adhesion Kinase (FAK) in CAF-mediated regulation of cancer cell metabolism.
- To investigate the impact of stromal FAK expression on patient survival and tumor growth.
Main Methods:
- Utilized mouse models of breast and pancreatic cancer with FAK-depleted CAFs.
- Performed proteomic, phosphoproteomic, and transcriptomic analyses.
- Investigated signaling pathways including chemokine-cytokine interactions and protein kinase A activation.
Main Results:
- Low FAK expression in the stromal compartment correlates with reduced overall survival in cancer patients.
- FAK depletion in CAFs promotes malignant cell glycolysis and tumor growth via paracrine signaling.
- FAK-depleted CAFs increase chemokine production, activating CCR1/CCR2 on cancer cells to enhance glycolysis.
Conclusions:
- FAK in CAFs is a critical regulator of cancer cell metabolism.
- Stromal FAK influences tumor growth and patient prognosis independently of cancer cell-intrinsic mutations.
- Targeting FAK in CAFs may offer a novel therapeutic strategy for cancer treatment.
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