PTEN deficiency and AMPK activation promote nutrient scavenging and anabolism in prostate cancer cells
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We report that PTEN-deficient prostate cancer cells use macropinocytosis to survive and proliferate under nutrient stress.PTEN loss increased macropinocytosis only in the context of AMPK activation revealing a general requirement for AMPK in macropinocytosis and a novel mechanism by which AMPK promotes survival under stress.In prostate cancer cells, albumin uptake did not require macropinocytosis, but necrotic cell debris proved a specific macropinocytic cargo.Isotopic labeling confirmed that macropinocytosed necrotic cell proteins fueled new protein synthesis in prostate cancer cells.Supplementation with necrotic debris, but not albumin, also maintained lipid stores suggesting that macropinocytosis can supply nutrients other than amino acids.Non-transformed prostatic epithelial cells were not macropinocytic, but patient-derived prostate cancer organoids and xenografts and autochthonous prostate tumors all exhibited constitutive macropinocytosis, and blocking macropinocytosis limited prostate tumor growth.Macropinocytosis of extracellular material by prostate cancer cells is a previously unappreciated tumor-microenvironment interaction that could be targeted therapeutically.
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Macropinocytosis utilizes necrotic cell debris as a fuel source, providing sugars, fatty acids, nucleotides, and amino acids to fuel cancer cell metabolism.
“Macropinocytosis has also been shown to utilize necrotic cell debris as a fuel source, which can provide sugars, fatty acids, nucleotides, and amino acids to fuel cancer cell metabolism233,234.”
From Pancreatic cancer: Advances and challenges (2023) · cites this paper as [233]
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From Pinocytosis to Methuosis—Fluid Consumption as a Risk Factor for Cell Death
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Macropinocytosis Renders a Subset of Pancreatic Tumor Cells Resistant to mTOR Inhibition
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Macropinocytosis and Cancer: From Tumor Stress to Signaling Pathways
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Akt and SGK protein kinases are required for efficient feeding by macropinocytosis
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Targeting Glutamine Metabolism in Prostate Cancer
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- Authors
- Kim, S. M., Nguyen, T. T., Ravi, A., Kubiniok, P., Finicle, B. T., Jayashankar, V., Malacrida, L., Hou, J., Robertson, J., Gao, D., Chernoff, J., Digman, M. A., Potma, E. O., Tromberg, B. J., Thibault, P., & Edinger, A. L.
- Affiliations
- University of California, Irvine (US)
- Université de Montréal (CA)
- Universidad de la República de Uruguay (UY)
- Chinese Academy of Sciences (CN)
- Fox Chase Cancer Center (US)
- ORCID
- Venue
- Cancer Discovery
- Published
- 2018-03-23
- Volume
- 8
- Issue
- 7
- Pages
- 866-883
- ISSN
- 2159-8274 (ISSN-L)
- 2159-8290
- PMC
- PMC6030497
- OpenAlex
- W2789786349
- Cited by
- 199
- References
- 70
- Citations by year
- 2026: 9 · 2025: 20 · 2024: 28 · 2023: 27 · 2022: 30 · 2021: 31 · 2020: 19 · 2019: 20 · 2018: 15
- FWCI
- 7.56
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cancer Discovery (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- HHS | National Institutes of Health (NIH) (GM089919, P30 CA62203, P41EB015890, P41-RR03155, P50-GM076516)
- Canada Research Chairs (Chaires de recherche du Canada)
- Genome Canada (Génome Canada)
- canada National Science and engineering research council (311598)
- Vanier Scholarship
- DOD | Congressionally Directed Medical Research Programs (CDMRP) (W81XWH-11-1-0535)
- American Cancer Society (ACS) (RSG-11-111-01-CDD)
- University of california cancer research coordinating committee (CRR-17-426826)
- UCI Applied Innovation (NA)
- US Department of Education (GAANN P200A120207)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Prostate Cancer Treatment and Research
- Keywords
- PTEN loss, AMPK activation, prostate cancer, nutrient scavenging, anabolism, cancer metabolism
- MeSH terms
- Nutrients, Animals, Humans, Male, Mice, Inbred C57BL, Pinocytosis, Prostatic Neoplasms, Stress, Physiological, Gene Deletion, PTEN Phosphohydrolase, Mice, AMP-Activated Protein Kinases
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