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Cited by 1,085Cancer, Hypoxia, and MetabolismMetabolism, Diabetes, and CancerPI3K/AKT/mTOR signaling in cancer

Tumor suppressors and cell metabolism: a recipe for cancer growth

Open access
Jones, Russell G., Thompson, Craig B.·2009·Genes & Development
DOI 10.1101/gad.1756509PMC PMC2763495
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Abstract

Growing tumors face two major metabolic challenges—how to meet the bioenergetic and biosynthetic demands of increased cell proliferation, and how to survive environmental fluctuations in external nutrient and oxygen availability when tumor growth outpaces the delivery capabilities of the existing vasculature. Cancer cells display dramatically altered metabolic circuitry that appears to directly result from the oncogenic mutations selected during the tumorigenic process. An emerging theme in cancer biology is that many of the genes that can initiate tumorigenesis are intricately linked to metabolic regulation. In turn, it appears that a number of well-established tumor suppressors play critical roles in suppressing growth and/or proliferation when intracellular supplies of essential metabolites become reduced. In this review, we consider the potential role of tumor suppressors as metabolic regulators.

AI snapshot

Written from the paper’s full text.

TL;DR

This review argues that oncogenic and tumor suppressor networks reprogram cancer cell metabolism to support growth and proliferation while also enabling adaptation to metabolic stress. It focuses on glycolysis, mitochondrial biosynthesis, AMPK, p53, HIF1, and autophagy as interconnected metabolic regulators in tumorigenesis.

Key findings

  • Proliferating cancer cells shift to aerobic glycolysis; >90% of pyruvate from glucose is converted to lactate by LDH-A, while the remaining ~10% enters mitochondria for biosynthetic pathways.
  • Tumor suppressors including p53, LKB1, TSC2, PTEN, VHL, SDH, FH, and Beclin-1 act as metabolic brakes or adaptation regulators, whereas oncogenes such as PI3K/Akt, c-Myc, and HIF1 promote nutrient uptake, glycolysis, biosynthesis, and survival.
  • AMPK is activated by energetic stress via LKB1 and can phosphorylate p53 at Ser-15, inducing a metabolic cell cycle checkpoint; in the absence of p53, metformin treatment delays tumor progression in cited work.
  • Autophagy is a conserved metabolic stress response and tumor suppressor mechanism; Beclin-1 haploinsufficiency promotes tumorigenesis in mouse models and is associated with breast and ovarian cancers in humans, and ~30% of cancers cannot be detected by FDG-PET.

Methods

  • Narrative review with no primary experimental data; it synthesizes literature on tumor suppressors and cell metabolism.
  • No sample, dataset, or statistical analysis is reported; the article cites 116 references.
  • Main analysis is a conceptual synthesis of oncogene/tumor suppressor signaling, metabolic pathways, and therapeutic implications.

Limitations

  • The paper states that it remains debated whether metabolic changes are a consequence or cause of tumorigenesis; the exact contribution of AMPK to tumor progression is unclear; the stimuli and target genes for p53-dependent metabolic responses remain to be determined; and the role of p53 in autophagy remains controversial.
  • Evident: as a narrative review, it does not systematically search or quantitatively synthesize evidence, and many mechanistic claims rely on cited studies rather than new data.
  • Evident: tumor heterogeneity and context dependence may limit generalizability; the paper notes that individual tumor cells could display distinct metabolic signatures and that ~30% of cancers are FDG-PET negative.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1101/gad.1756509

Cites

119 of 119 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

0 of 65 cited sources checked · 0 supported · 0 flagged

  • Premisecitation
    § Tumor suppressors and cell metabolism: a recipe for cancer growth

    Tumor cells often display fundamental changes in pathways of energy metabolism and nutrient uptake.

    “tumor cells, in order to meet the increased requirements of proliferation, often display fundamental changes in pathways of energy metabolism and nutrient uptake (Garber 2006).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites Garber 2006

      Not checked in the free run.

  • Premisecitation
    § Tumor suppressors and cell metabolism: a recipe for cancer growth

    Tumor cells preferentially use glycolysis over mitochondrial oxidative phosphorylation for glucose-dependent ATP production even in the presence of ample oxygen (the Warburg effect).

    “tumor cells preferentially use glycolysis over mitochondrial oxidative phosphorylation (OXPHOS) for glucose-dependent ATP production even in the presence of ample oxygen to fuel mitochondrial respiration, a phenomenon known as the ''Warburg effect'' (Warburg 1956).”
    • Also stated in: § Glycolysis-metabolic reprogramming fuels cell growth and proliferation · plain
      “One of the primary metabolic changes associated with proliferating tumor cells is induction of aerobic glycolysis (Fig. 1).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites Warburg 1956

      Not checked in the free run.

  • Interpretationreasoning
    § Tumor suppressors and cell metabolism: a recipe for cancer growth

    Alterations in cellular metabolism may contribute to the malignant phenotype.

    “supporting the theory that alterations in cellular metabolism may contribute to the malignant phenotype.”
    Quote in the paperSubstantial claim
  • Interpretationnone given

    AMPK functions across evolution as a low energy checkpoint, triggering multiple biological adaptations designed to preserve energy and adapt to metabolic stress before the cell reaches a state of bioenergetic catastrophe that triggers cell death.

    “AMPK appears to function across evolution as a low energy checkpoint, triggering multiple biological adaptations designed to preserve energy and adapt to metabolic stress before the cell reaches a state of bioenergetic catastrophe that triggers cell death.”
    Quote in the paperNot a substantial claim
  • Interpretationreasoning

    Despite the low overall percentage of pyruvate available for mitochondrial synthesis, the high rate of glycolytic flux provides sufficient amounts for biosynthesis.

    “Despite the low overall percentage of pyruvate available for mitochondrial synthesis, the high rate of glycolytic flux provides sufficient amounts for biosynthesis.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: The remaining pyruvate from aerobic glycolysis that is not converted to lactate (~10% of total) enters the mitochondrion and is extruded from the TCA cycle at various steps for use in biosynthetic pathways.
  • May combine two claims. 16
  • Classified as probably not a substantial claim. 6

  • May combine two claims.

    Premisecitation
    § Tumor suppressors and cell metabolism: a recipe for cancer growth

    Enhanced glucose uptake visualized by FDG-PET correlates with poor prognosis and higher metabolic potential in many tumor types.

    “Enhanced glucose uptake visualized by FDG-PET correlates with poor prognosis and higher metabolic potential in many tumor types (Gatenby and Gillies 2004;Kroemer and Pouyssegur 2008)”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites Gatenby and Gillies 2004

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    • cites Kroemer and Pouyssegur 2008

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  • May combine two claims.

    Interpretationreasoning
    § Tumor suppressors and cell metabolism: a recipe for cancer growth

    Tumors face two distinct metabolic challenges: (1) how to modify cellular metabolism to support enhanced cell growth and proliferation, and (2) how to engage strategies of metabolic adaptation to survive periods of metabolic stress and maintain viability as cells accumulate.

    “Thus, tumors face two distinct metabolic challenges: (1) how to modify their cellular metabolism to support enhanced cell growth and proliferation, and (2) how to engage strategies of metabolic adaptation to survive periods of metabolic stress and maintain viability as the cells accumulate.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    AMPK is responsive to changes in the cellular AMP:ATP ratio and is activated by stresses that stimulate ATP consumption or inhibit ATP production.

    “AMPK is responsive to changes in the cellular AMP:ATP ratio and is activated by stresses that stimulate ATP consumption or inhibit ATP production (Hardie 2003).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Hardie 2003

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Oncogenic c-Myc promotes increased aerobic glycolysis through the constitutive elevation of LDH-A, as well as expression of enzymes involved in nucleotide and amino acid metabolism.

    “Oncogenic c-Myc promotes increased aerobic glycolysis through the constitutive elevation of LDH-A (Shim et al. 1997;Osthus et al. 2000), as well as expression of enzymes involved in nucleotide and amino acid metabolism (Gordan et al. 2007).”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites Shim et al. 1997

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    • cites Osthus et al. 2000

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    • cites Gordan et al. 2007

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  • May combine two claims.

    Premisecitation
    § Tumor suppressors and cell metabolism: a recipe for cancer growth

    The fundamental metabolic switch (metabolic transformation) may confer a selective growth advantage and/or resistance to apoptosis to allow cancer cells to maintain mitochondrial bioenergetics and integrity during cell growth and proliferation.

    “This fundamental metabolic switch (''metabolic transformation'') may confer a selective growth advantage and/or resistance to apoptosis to allow cancer cells to maintain mitochondrial bioenergetics and integrity during cell growth and proliferation (DeBerardinis et al. 2008).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites DeBerardinis et al. 2008

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Activity of the PI3K pathway is deregulated in cancer through activating mutations in PI3K or PTEN loss.

    “Activity of the pathway is deregulated in cancer through a variety of mechanisms, including activating mutations in PI3K (Samuels et al. 2004(Samuels et al. , 2005;;Jia et al. 2008) or PTEN loss (Cairns et al. 1997).”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites Samuels et al. 2004

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    • cites Samuels et al. 2005

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    • cites Jia et al. 2008

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  • May combine two claims.

    Premisecitation

    Inhibition of ACL results in decreased glucose-dependent lipid synthesis and impaired cell proliferation.

    “Inhibition of ACL results in decreased glucose-dependent lipid synthesis and impaired cell proliferation (Hatzivassiliou et al. 2005).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites Hatzivassiliou et al. 2005

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  • May combine two claims.

    Premisecitation

    Protein translation is essential for tumor growth, and deregulated translation itself can be tumorigenic.

    “Protein translation is essential for tumor growth, and deregulated translation itself can be tumorigenic (Mamane et al. 2004).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites Mamane et al. 2004

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Myc transformed cells are exquisitely sensitive to glutamine levels and rapidly deplete their TCA cycle intermediates when glutamine availability is reduced.

    “Interestingly, Myc transformed cells are exquisitely sensitive to glutamine levels and rapidly deplete their TCA cycle intermediates when glutamine availability is reduced (Yuneva et al. 2007).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Yuneva et al. 2007

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    TORC1 activity is kept in check by the tumor suppressors TSC1/TSC2 and LKB1, which block mTOR activation through inhibition of Rheb; mutation of these genes leads to elevated mTOR activity and the development of hamartomas.

    “TORC1 activity is kept in check by the tumor suppressors TSC1/ TSC2 and LKB1, which function to block mTOR activation through inhibition of the small GTPase Rheb; mutation of these genes leads to elevated mTOR activity and the development of hamartomas (Inoki et al. 2003;Corradetti et al. 2004;Shaw et al. 2004a).”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites Inoki et al. 2003

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    • cites Corradetti et al. 2004

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    • cites Shaw et al. 2004a

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  • May combine two claims.

    Interpretationnone given

    Major physiological strategies of metabolic adaptation include cell cycle inhibition, inhibition of biosynthetic pathways, increases in bioenergetic pathways, and induction of autophagy.

    “Major physiological strategies of metabolic adaptation include cell cycle inhibition, inhibition of biosynthetic pathways (lipid, protein synthesis), increases in bioenergetic pathways (b-oxidation, glycolysis, and OXPHOS), and induction of autophagy.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S4 (based).

    Interpretationnone given

    HIF1a blocks pyruvate entry into the mitochondrion by up-regulating the PDH antagonist PDK1.

    “HIF1a blocks pyruvate entry into the mitochondrion by up-regulating the PDH antagonist PDK1.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Interpretationnone given

    AMPK mediates metabolic adaptation through down-regulation of fatty acid synthesis through inhibition of ACC1, translation inhibition by blocking TORC1 activity, and activation of p53.

    “AMPK mediates metabolic adaptation through several pathways, including down-regulation of fatty acid synthesis through inhibition of ACC1, translation inhibition by blocking TORC1 activity, and activation of p53.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationnone given

    Transcriptional regulation of DRAM by p53 induces autophagy, the products of which can also fuel OXPHOS.

    “Transcriptional regulation of DRAM by p53 induces autophagy, the products of which can also fuel OXPHOS.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S4 (based).

    Interpretationnone given

    Failure to manage or correct bioenergetic imbalance leads to cytochrome c release from mitochondria and induction of apoptosis.

    “Failure to manage or correct bioenergetic imbalance leads to cytochrome c release from mitochondria and induction of apoptosis.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    UVRAG and Bif display tumor suppressor properties.

    “Other modifiers of Beclin-1 activity such as UVRAG and Bif display tumor suppressor properties (C.Liang et al. 2007;Takahashi et al. 2007)”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites C.Liang et al. 2007 source

      Not checked in the free run.

    • cites Takahashi et al. 2007

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  • May combine two claims.

    Premisecitation

    AMPK phosphorylates p53 at Ser-15, which stimulates both its transcriptional activity and initiates a metabolic cell cycle checkpoint.

    “AMPK phosphorylates p53 at Ser-15, which stimulates both its transcriptional activity and initiates a metabolic cell cycle checkpoint (Jones et al. 2005).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites Jones et al. 2005

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S4 (based).

    Interpretationnone given

    Bioenergetic stress activates AMPK through an LKB-dependent manner.

    “Bioenergetic stress activates AMPK through an LKB-dependent manner.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S4 (based).

    Interpretationnone given

    Low HIF1a protein levels are maintained in cells under normoxia through VHL-mediated proteosomal degradation.

    “Low HIF1a protein levels are maintained in cells under normoxia through the action of VHL-mediated proteosomal degradation.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based).

    Interpretationnone given

    Rag GTPases regulate TORC1 activity and autophagy in response to amino acid deprivation.

    “Rag GTPases regulate TORC1 activity and autophagy in response to amino acid deprivation.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based).

    Interpretationreasoning

    Inability to induce autophagy under conditions of nutrient or oxygen deprivation could render tumors more susceptible to apoptosis by metabolic stress.

    “However, any subsequent inability to induce autophagy under conditions of nutrient or oxygen deprivation could render tumors more susceptible to apoptosis by metabolic stress.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Interpretationreasoning

    LKB or p53 deficiency, while permissive for unchecked cell growth, renders cells more susceptible to death by metabolic stress.

    “LKB or p53 deficiency, while permissive for unchecked cell growth, renders cells more susceptible to death by metabolic stress.”
    Quote in the paperSubstantial claim
22 of 22

  • The paper relies on this without support.

    In proliferating cancer cells, the majority (>90%) of pyruvate generated from glucose is converted to lactate by LDH-A and secreted rather than oxidized to completion.

    “In proliferating cancer cells, the majority of the pyruvate generated from glucose (>90%) is converted to lactate by lactate dehydrogenase (LDH-A), where it is readily secreted into the extracellular environment rather than oxidized to completion.”

  • The paper relies on this without support.

    Metabolism of glucose through the oxidative or nonoxidative arms of the pentose phosphate pathway generates ribose-5-phosphate, a key intermediate in nucleotide biosynthesis.

    “Metabolism of glucose through the oxidative or nonoxidative arms of the pentose phosphate pathway (PPP) generates ribose-5phosphate (Rib-5-P), a key intermediate in nucleotide biosynthesis.”

  • The paper relies on this without support.

    The oxidative arm of the PPP can produce NADPH, which supplies a pool of reducing equivalents for both nucleotide and fatty acid biosynthesis.

    “The oxidative arm of the PPP can also produce NADPH, which supplies a pool of reducing equivalents for both nucleotide and fatty acid biosynthesis.”

  • The paper relies on this without support.

    Pyruvate can be imported into the mitochondria and converted into substrates for the production of additional amino acids or fatty acid synthesis, and used to maintain mitochondrial membrane potential.

    “Finally, pyruvate can be imported into the mitochondria and converted into substrates for the production of additional amino acids or fatty acid synthesis, and used to maintain mitochondrial membrane potential.”

  • The paper relies on this without support.

    The remaining pyruvate from aerobic glycolysis that is not converted to lactate (~10% of total) enters the mitochondrion and is extruded from the TCA cycle at various steps for use in biosynthetic pathways.

    “The remaining pyruvate from aerobic glycolysis that is not converted to lactate (;10% of total) enters the mitochondrion and is extruded from the TCA cycle at various steps for use in biosynthetic pathways.”

  • The paper relies on this without support.

    A solid tumor can outstrip its nutrient and oxygen supply as it grows, resulting in metabolic stress.

    “A solid tumor can outstrip its nutrient and oxygen supply as it grows, resulting in metabolic stress (tumors experiencing metabolic stress are depicted in gray).”

  • The paper relies on this without support.

    Tumor cells must undergo a period of metabolic adaptation to survive metabolic stress or undergo apoptosis.

    “As a consequence, tumor cells must undergo a period of metabolic adaptation to survive this metabolic stress or undergo apoptosis.”

  • The paper relies on this without support.

    PI3K is a central regulator of metabolism in both nontransformed and transformed cells.

    “A central regulator of metabolism in both nontransformed and transformed cells is the phosphatidylinositol 3-kinase (PI3K), a lipid kinase that regulates the levels of phosphorylated phosphatidylinositol (PIP 3 ) at the plasma membrane.”

  • The paper relies on this without support.

    Growth factor-dependent activation of PI3K leads to activation of downstream effectors including Akt and mTOR that coordinate metabolic activities supporting cellular biosynthesis.

    “Growth factor-dependent activation of PI3K leads to the activation of downstream effectors including Akt and the mammalian target of rapamycin (mTOR) that coordinate metabolic activities that support cellular biosynthesis.”

  • The paper relies on this without support.

    mTOR coordinates protein synthesis by regulating amino acid uptake, tRNA charging, and translation initiation.

    “mTOR coordinates protein synthesis by regulating amino acid uptake, tRNA charging, and translation initiation.”

  • The paper relies on this without support.

    Myc is a transcription factor activated by growth factor stimulation and is essential for the regulation of proliferation and cell cycle entry in nontransformed cells.

    “Myc is a transcription factor activated by growth factor stimulation and is essential for the regulation of proliferation and cell cycle entry in nontransformed cells.”

  • The paper relies on this without support.

    AMPK is activated under conditions of energetic stress, such as that triggered by nutrient deprivation or hypoxia.

    “As a cellular sensor of AMP levels, AMPK is activated under conditions of energetic stress, such as that triggered by nutrient deprivation or hypoxia.”

  • The paper relies on this without support.

    Beclin-1 is required for autophagy induction in mammalian cells.

    “Studies involving Beclin-1, which is required for autophagy induction in mammalian cells, suggest that autophagy functions as an important tumor suppressor mechanism.”

  • The paper relies on this without support.

    SDH and FH function as tumor suppressors in humans.

    “However, the fact that metabolic enzymes such as SDH and FH function as tumor suppressors in humans suggests that metabolic deregulation can be an initiating event in cancer.”

  • The paper relies on this without support.

    Cancer cells can become dependent on the activity of a specific oncogene for function and survival (oncogene addiction).

    “In cancer cells, a given transformation event (i.e., oncogene activation) may play a qualitatively different or essential role in a given pathway compared with its role in normal cells, such that cancer cells become dependent on the activity of a specific oncogene for function and survival, a concept known as oncogene addiction.”
15 of 15

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Cancer cells preferentially use glycolysis instead of respiration to obtain energy (Warburg effect).

    “It is known that cancer cells preferentially use glycolysis instead of respiration to obtain energy (Warburg effect) (20).”

    From Mitochondrial Dysfunction Contributes to Oncogene-Induced Senescence (2009) · cites this paper as [20]

  • Cellular transformation is a multistep process requiring acquisition of activated oncogenes and loss of tumor-suppressor genes, leading to usurpation of cellular signaling pathways controlling proliferation, survival, and metabolism.

    “Cellular transformation is a multistep process requiring acquisition of activated oncogenes and loss of tumor-suppressor genes, leading to usurpation of cellular signaling pathways controlling proliferation, survival, and metabolism 65, 66.”

    From Mitochondrial reactive oxygen species regulate cellular signaling and dictate biological outcomes (2010) · cites this paper as [66]

  • Tumor-promoting mutations in oncogenes and tumor suppressors tend to converge on a metabolic phenotype of enhanced glycolysis and energy production, contributing to self-sufficiency of growth and evasion of growth-suppressive signals.

    “Tumor-promoting mutations in these genes tend to converge on a metabolic phenotype of enhanced glycolysis and energy production, thereby contributing to self-sufficiency of growth and evasion of growth-suppressive signals.”

    From Cellular Metabolism and Disease: What Do Metabolic Outliers Teach Us? (2012) · cites this paper as Jones and Thompson, 2009

  • Many human oncogenes and tumor suppressors regulate glucose metabolism.

    “First, many human oncogenes and tumor suppressors regulate glucose metabolism (Figure 3A) (DeBerardinis, 2008; Jones and Thompson, 2009).”

    From Cellular Metabolism and Disease: What Do Metabolic Outliers Teach Us? (2012) · cites this paper as Jones and Thompson, 2009

Cites

1 retracted

Flagged first, then by citations

3 of the 122 references couldn’t be matched to a known paper.

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Related

Authors
Jones, R. G., & Thompson, C. B.
Affiliations
  • McGill University (CA)
  • Abramson Cancer Center (US)
ORCID
Venue
Genes & Development
Publisher
Cold Spring Harbor Laboratory
Published
2009-03-01
Volume
23
Issue
5
Pages
537-548
ISSN
  • 0890-9369 (ISSN-L)
  • 1549-5477
DOI
10.1101/gad.1756509
PMC
PMC2763495
OpenAlex
W2127049578
Semantic Scholar
f40e1cdc46be710b4cc935547b39b521d22208fa
Cited by
1,085
References
122
Citations by year
2026: 11 · 2025: 39 · 2024: 30 · 2023: 54 · 2022: 50 · 2021: 63 · 2020: 56 · 2019: 66 · 2018: 69 · 2017: 68 · 2016: 69 · 2015: 78 · 2014: 100 · 2013: 97 · 2012: 87
Type
posted content
Language
en
Open access
Locations
  • Genes & Development (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • McGill University
  • National Institutes of Health
  • Canadian Institutes of Health Research
  • National Cancer Institute (R01CA105463)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
  • 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
Keywords
tumor suppressor, cancer metabolism, tumor growth, oncogenic mutations, metabolic regulation, cell proliferation, nutrient availability, oxygen availability, tumor vasculature, biosynthesis, bioenergetics
MeSH terms
Animals, Autophagy, Cells, Glycolysis, Humans, Mitochondria, Neoplasms, Oncogenes, Signal Transduction, Genes, Tumor Suppressor, Cell Proliferation, AMP-Activated Protein Kinases

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