Pathway link MTORC2-LIPID
mTORC2 Lipid synthesis
mTORC2 activates Lipid synthesis.
mTORC2 also drives fat-making, which is one of the ways it is thought to help tumours grow. The cause-and-effect part was shown in mice; in people with liver cancer, the study only found that more fat-making went together with higher mTORC2 activity.
The conditions it holds under
The causal part comes from mouse liver: one liver tumour model (GUR2017) that progresses from steatosis to hepatocellular carcinoma, and liver-specific Rictor knockout in otherwise normal mice (HAG2012), where loss of mTORC2 lowered lipogenesis through Akt and SREBP1c. GUR2017 also reports that in human HCC, increased lipogenesis correlated with elevated mTORC2 activity: correlative human data, not a test of this step. Not established as a general mTORC2 function outside liver.
- Time it takes
- long exposure (days to weeks)
- Step
- indirect (through steps not drawn here)
- Measured in
- mouse
- Reaches people?
- plausible in people, not shown directly
- How settled
- emerging, few independent studies
Studies behind it
| Year | Evidence | Study |
|---|---|---|
| 2017 | A | mTORC2 Promotes Tumorigenesis via Lipid SynthesisGUR2017 mTORC2 promotes tumorigenesis through control of de novo lipid synthesis. |
| 2012 | A | Hepatic mTORC2 activates glycolysis and lipogenesis through Akt, glucokinase, and SREBP1cHAG2012 The authors deleted rictor, an essential mTORC2 component, only in mouse liver. In fed knockout mice the liver lost Akt Ser473 phosphorylation and had lower glucokinase and SREBP1c activity, so it kept making glucose (gluconeogenesis) while glycolysis and fat synthesis fell, as if it could not sense that the animal had eaten. The mice became hyperglycaemic and hyperinsulinaemic with low blood lipids. In mTORC2-deficient hepatocytes, constitutively active Akt2 restored both glucose flux and lipogenesis, while extra glucokinase restored glucose flux but not lipogenesis, placing Akt as the main route from hepatic mTORC2 to these outputs. Boundary: Mouse liver with lifelong genetic loss of mTORC2, plus cultured mouse hepatocytes. Not a drug study and not tested in people. Drafted from the abstract only. |
Points the other way
No study in the Atlas contradicts this link. That means none in this curated set, not none in the literature.
Who has checked this
- Checked by
- No researcher outside the project has checked this link yet.
- Curator sign-off
- Not signed off yet. This link was drafted with AI help and has not been reviewed link by link; treat it as a proposal until it is.
- Curated by
- Oliver Barton, with AI help for drafting; see how links are checked.
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