mTORC2 Promotes Tumorigenesis via Lipid Synthesis
What this study shows
mTORC2 promotes tumorigenesis through control of de novo lipid synthesis.
At a glance
| Evidence type | A Animal model Marked A because it is an animal intervention or observation study measuring an organismal outcome (model: Mouse; cells); the code names the system studied -- animal work can be rigorous and still not be human data. |
| Study type | 4 - Animal Study |
| Model system | Mouse; cells |
| Journal | Cancer cell |
| Year | 2017 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1016/j.ccell.2017.11.011 · PMID 29232555 |
Extracted findings
These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.
| Intervention | Genetic mTOR-driven mouse model |
| Target | mTORC2 |
| Model | Mouse; cells |
| Effect | Hepatic mTORC2 promotes de novo fatty-acid/lipid synthesis (sphingolipids, glycerophospholipids) driving steatosis → hepatocellular carcinoma |
In the Atlas
Related topics
Links in the pathway map
- Supports mTORC2 activates Lipid synthesis
More studies on this topic
- Activation of a metabolic gene regulatory network downstream of mTOR complex 1 (2010)
- Hepatic mTORC2 activates glycolysis and lipogenesis through Akt, glucokinase, and SREBP1c (2012)
- Sterol regulatory element-binding proteins are essential for the metabolic programming of effector T cells and adaptive immunity (2013)
- Malonyl-CoA is a conserved endogenous ATP-competitive mTORC1 inhibitor (2023)
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