Metabolic Reprogramming of Stromal Fibroblasts through p62-mTORC1 Signaling Promotes Inflammation and Tumorigenesis
Open accessAbstract
The tumor microenvironment plays a critical role in cancer progression, but the precise mechanisms by which stromal cells influence the epithelium are poorly understood. Here we show that p62 levels were reduced in the stroma of several tumors and that its loss in the tumor microenvironment or stromal fibroblasts resulted in increased tumorigenesis of epithelial prostate cancer cells. The mechanism involves the regulation of cellular redox through an mTORC1/c-Myc pathway of stromal glucose and amino acid metabolism, resulting in increased stromal IL-6 production, which is required for tumor promotion in the epithelial compartment. Thus, p62 is an anti-inflammatory tumor suppressor that acts through the modulation of metabolism in the tumor stroma.
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Metabolic dysregulation of CAFs may be coupled to altered immunoregulation, possibly through IL-6 production or depletion of immunomodulating amino acids.
“Furthermore, metabolic dysregulation of CAFs may also be coupled to altered immunoregulation, possibly through IL-6 production or depletion of immunomodulating amino acids128,132.”
From A framework for advancing our understanding of cancer-associated fibroblasts (2020) · cites this paper as [128]
The Discussion states that metabolic reprogramming in the tumor stroma creates an IL-6-driven inflammatory environment, supporting the IL-6 route. The Results section on p62, ROS, and IL-6 discusses altered amino-acid metabolism but does not show depletion of immunomodulating amino acids as a route to altered immunoregulation. (LLM, conf=0.86)
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- Authors
- Valencia, T., Kim, J. Y., Abu-Baker, S., Moscat-Pardos, J., Ahn, C. S., Reina-Campos, M., Duran, A., Castilla, E. A., Metallo, C. M., Diaz-Meco, M. T., & Moscat, J.
- Affiliations
- Sanford Burnham Prebys Medical Discovery Institute (US)
- University of California San Diego (US)
- University of Cincinnati (US)
- Corresponding author
- Moscat, Jorge
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2014-07
- Volume
- 26
- Issue
- 1
- Pages
- 121-135
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC4101061
- OpenAlex
- W2113240092
- Cited by
- 304
- References
- 62
- Citations by year
- 2026: 6 · 2025: 17 · 2024: 13 · 2023: 12 · 2022: 29 · 2021: 41 · 2020: 37 · 2019: 34 · 2018: 28 · 2017: 27 · 2016: 31 · 2015: 23 · 2014: 6
- FWCI
- 9.29
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Cancer Institute (R01CA132847, R01CA172025, R01CA134530, P30CA030199)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Keywords
- p62, mTORC1, stromal fibroblasts, tumor microenvironment, metabolic reprogramming, prostate cancer, c-Myc, interleukin-6, inflammation, carcinogenesis, redox regulation, glucose metabolism, amino acid metabolism, tumor stroma
- MeSH terms
- Sequestosome-1 Protein, Mechanistic Target of Rapamycin Complex 1, Amino Acids, Animals, Cell Communication, Cell Transformation, Neoplastic, Energy Metabolism, Fibroblasts, Glucose, Heat-Shock Proteins, Humans, Inflammation, Male, Mice, Inbred C57BL, Neoplasm Invasiveness, Prostatic Hyperplasia, Prostatic Neoplasms, Time Factors, Transfection, Signal Transduction, Interleukin-6, Proto-Oncogene Proteins c-myc, Stromal Cells, Mice, Knockout, Oxidative Stress, Inflammation Mediators, Coculture Techniques, Prostatic Intraepithelial Neoplasia, RNA Interference, Cell Line, Tumor, Multiprotein Complexes, Adaptor Proteins, Signal Transducing, PTEN Phosphohydrolase, Mice, HEK293 Cells, TOR Serine-Threonine Kinases, Tumor Microenvironment
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