Cited by 306Cancer, Hypoxia, and MetabolismPI3K/AKT/mTOR signaling in cancerImmune cells in cancer

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Metabolic Reprogramming of Stromal Fibroblasts through p62-mTORC1 Signaling Promotes Inflammation and Tumorigenesis

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Valencia, Tania, Kim, Ji Young, Abu-Baker, Shadi, Moscat-Pardos, Jorge, Ahn, Christopher S., Reina-Campos, Miguel, Duran, Angeles, Castilla, Elias A., Metallo, Christian M., Diaz-Meco, Maria T., Moscat, Jorge·2014·Cancer Cell

DOI 10.1016/j.ccr.2014.05.004PMC PMC4101061

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Abstract

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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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
ORCID: Ahn, Christopher S.
Metallo, Christian M.
Moscat, Jorge
Venue: Cancer Cell
Publisher: Elsevier BV
Published: 2014-07
Volume: 26
Issue: 1
Pages: 121-135
ISSN: 1535-6108 (ISSN-L)
DOI: 10.1016/j.ccr.2014.05.004
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: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 465 d)
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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Metabolic Reprogramming of Stromal Fibroblasts through p62-mTORC1 Signaling Promotes Inflammation and Tumorigenesis

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