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Insulin–PI3K signalling: an evolutionarily insulated metabolic driver of cancer
Open accessAbstract
Cancer is driven by incremental changes that accumulate, eventually leading to oncogenic transformation. Although genetic alterations dominate the way cancer biologists think about oncogenesis, growing evidence suggests that systemic factors (for example, insulin, oestrogen and inflammatory cytokines) and their intracellular pathways activate oncogenic signals and contribute to targetable phenotypes. Systemic factors can have a critical role in both tumour initiation and therapeutic responses as increasingly targeted and personalized therapeutic regimens are used to treat patients with cancer. The endocrine system controls cell growth and metabolism by providing extracellular cues that integrate systemic nutrient status with cellular activities such as proliferation and survival via the production of metabolites and hormones such as insulin. When insulin binds to its receptor, it initiates a sequence of phosphorylation events that lead to activation of the catalytic activity of phosphoinositide 3-kinase (PI3K), a lipid kinase that coordinates the intake and utilization of glucose, and mTOR, a kinase downstream of PI3K that stimulates transcription and translation. When chronically activated, the PI3K pathway can drive malignant transformation. Here, we discuss the insulin-PI3K signalling cascade and emphasize its roles in normal cells (including coordinating cell metabolism and growth), highlighting the features of this network that make it ideal for co-option by cancer cells. Furthermore, we discuss how this signalling network can affect therapeutic responses and how novel metabolic-based strategies might enhance treatment efficacy for cancer.
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“Although not covered in this review, the importance of aberrant functions of different PLCs and PI3Ks in disease development is well established and continues to expand [11,62,67,72,134–138].”
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“p110α heterodimers play a key role in glucose homeostasis and in insulin and growth factor signalling [65–67].”
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Metadata
- Authors
- Hopkins, B. D., Goncalves, M. D., & Cantley, L. C.
- Affiliations
- Icahn School of Medicine at Mount Sinai (US)
- Weill Cornell Medicine (US)
- Corresponding author
- Hopkins, Benjamin D.
- Venue
- Nature Reviews Endocrinology
- Published
- 2020-03-03
- Volume
- 16
- Issue
- 5
- Pages
- 276-283
- ISSN
- 1759-5029 (ISSN-L)
- 1759-5037
- PMC
- PMC7286536
- OpenAlex
- W3009258273
- Cited by
- 288
- References
- 78
- Citations by year
- 2026: 34 · 2025: 50 · 2024: 46 · 2023: 52 · 2022: 45 · 2021: 41 · 2020: 20
- FWCI
- 3.81
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature Reviews Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (K08CA230318, R00CA230384, R35CA197588)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Keywords
- insulin signaling, PI3K signaling, mTOR, oncogenic transformation, cancer metabolism, insulin resistance, insulin receptor, cancer therapy resistance, metabolic targeting, tumor initiation
- MeSH terms
- Animals, Endocrine System, Biological Evolution, Humans, Insulin, Neoplasms, Signal Transduction, Phosphatidylinositol 3-Kinases
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