Cited by 358PI3K/AKT/mTOR signaling in cancerMetabolism, Diabetes, and CancerProtein Kinase Regulation and GTPase Signaling

Oncogenic Roles of the PI3K/AKT/mTOR axis

Aoki, Masahiro, Fujishita, Teruaki·2017·Current topics in microbiology and immunology

Abstract

The PI3K/AKT/mTOR pathway is frequently activated in various human cancers and has been considered a promising therapeutic target. Many of the positive regulators of the PI3K/AKT/mTOR axis, including the catalytic (p110α) and regulatory (p85α), of class IA PI3K, AKT, RHEB, mTOR, and eIF4E, possess oncogenic potentials, as demonstrated by transformation assays in vitro and by genetically engineered mouse models in vivo. Genetic evidences also indicate their roles in malignancies induced by activation of the upstream oncoproteins including receptor tyrosine kinases and RAS and those induced by the loss of the negative regulators of the PI3K/AKT/mTOR pathway such as PTEN, TSC1/2, LKB1, and PIPP. Possible mechanisms by which the PI3K/AKT/mTOR axis contributes to oncogenic transformation include stimulation of proliferation, survival, metabolic reprogramming, and invasion/metastasis, as well as suppression of autophagy and senescence. These phenotypic changes are mediated by eIF4E-induced translation of a subset of mRNAs and by other downstream effectors of mTORC1 including S6K, HIF-1α, PGC-1α, SREBP, and ULK1 complex.

Integrity signals

Registry

Crossref · 10.1007/82_2017_6

Cites

229 of 229 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

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?

  • Constitutive activation of oncogene-driven signaling pathways may activate hypoxia signaling independently of oxygen supply.

    “However, constitutive activation of oncogene-driven signaling pathways may also activate hypoxia signaling independently of oxygen supply.”
  • Activating mutations in growth factor receptors or their signaling pathways (EGFR, HER2, RAS, BRAF, PI3KCA/AKT) are characteristic for many cancer types.

    “Mutations of growth factor receptors or members of their respective signaling pathways are characteristics for many different cancer types: EGFR mutations in lung adenocarcinoma, HER2 amplifications in breast and gastric cancers, RAS mutations in lung and colorectal cancers, BRAF mutations in melanoma, thyroid or GI-tract cancers or mutations of the lipid kinase signaling pathway members (PI3KCA,”

Cites

1 retracted

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Aoki, M., & Fujishita, T.
Affiliations
Aichi Cancer Center Research Institute (JP)
Corresponding author
Aoki, Masahiro
Venue
Current topics in microbiology and immunology
Published
2017
Volume
407
Pages
153-189
ISSN
  • 0070-217X (ISSN-L)
  • 2196-9965
OpenAlex
W2617686875
Cited by
355
References
228
Citations by year
2026: 6 · 2025: 18 · 2024: 40 · 2023: 61 · 2022: 91 · 2021: 65 · 2020: 45 · 2019: 21 · 2018: 7 · 2017: 1
FWCI
25.23
Type
book chapter
Language
en
Open access
closed
Locations
  • Current topics in microbiology and immunology (publishedVersion)
  • PubMed (publishedVersion)
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 › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
Keywords
PI3K/AKT/mTOR pathway, oncogenic transformation, class IA PI3K, Akt, Rheb, mTOR, eIF4E, PTEN, TSC1/2, LKB1, receptor tyrosine kinase, Ras, metabolic reprogramming, invasion and metastasis, autophagy inhibition, cellular senescence, mTORC1, S6K, HIF-1α, PGC-1α, SREBP, ULK1, cancer therapy targets
MeSH terms
Animals, Cell Transformation, Neoplastic, Humans, Signal Transduction, Phosphatidylinositol 3-Kinases, Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review