Journal September 26, 2026 5 min read

What is the mTOR pathway?

MTOR is a serine/threonine kinase that sits at the centre of a signalling network controlling cell growth, proliferation and metabolism. This page outlines what the pathway is and what laboratory research has reported ab

peptides-pro Editorial

mTOR — mechanistic target of rapamycin — is a serine/threonine protein kinase that functions as the catalytic core of two distinct multi-protein complexes, mTORC1 and mTORC2. It is the defining node of the PI3K/Akt/mTOR signalling axis, a pathway that integrates nutrient, energy and growth-factor signals to regulate protein synthesis, autophagy, lipid metabolism and cell-cycle progression. In the research literature the pathway is referred to interchangeably as mTOR, PI3K/Akt/mTOR, or PI3K-Akt-mTOR depending on which arm of the cascade a given study interrogates.

The work summarised below centres on the PI3K/Akt/mTOR kinase cascade and its upstream regulators, including PTEN, and on the receptor tyrosine kinase input to that cascade, notably c-MET.

Research Studies

LL-37 and SQLE-mediated cholesterol synthesis in osteosarcoma cells

LL-37, the human cathelicidin peptide, was examined in osteosarcoma (OS) cell lines alongside normal human bone marrow mesenchymal stem cells (hBMSCs). In vitro assays covered viability, clonogenic survival, migration, invasion, cell-cycle distribution, cell death and cholesterol metabolism, with transcriptomic profiling and siRNA-mediated knockdown used to probe mechanism. The study reported that LL-37 inhibited osteosarcoma progression by suppressing SQLE-mediated cholesterol synthesis via the PTEN/AKT/mTOR pathway [1]. The findings are in vitro; no animal or human outcome data are reported in the evidence available here.

mTOR pathway signalling and intramuscular fat deposition in Yanbian yellow cattle

Sixty 24-month-old Yanbian yellow cattle (n = 30 per group), reared under standardised environmental and dietary conditions, were assigned to high-intramuscular-fat (HM) and low-intramuscular-fat (LM) groups. HM beef showed significantly higher intramuscular fat (P < 0.05), increased monounsaturated fatty acids and reduced saturated fatty acids relative to LM. Integrated transcriptomics and non-targeted metabolomics (n = 8 per group) associated intramuscular fat deposition with a dual-layered regulatory framework: an upstream signalling layer comprising PPAR, PI3K-Akt and mTOR pathways, and a downstream metabolic execution layer [2]. This is a livestock production study; the observations describe pathway association with a production trait rather than a pharmacological intervention.

Alpha ketoglutarate and inflammatory response in colorectal cancer surgery

The RISIS-CR trial proposes to identify inflammatory responsiveness in patients prior to colorectal cancer (CRC) surgery and to administer prophylactic anti-inflammatory treatment targeted only to those mounting an excessive pro-inflammatory response, on the stated rationale that personalised selection avoids further suppressing immune function in patients who are already immunocompromised. The proposal describes alpha ketoglutarate (AKG), a geroprotector supplement, as the candidate intervention, noting that geroprotectors reduce inflammation and may reduce postoperative systemic inflammatory response and complications after CRC surgery [3]. This is a registered trial protocol; the evidence block does not report results.

Fingolimod and interstitial fibrosis after kidney transplantation

A randomised, double-blind, placebo-controlled trial in de novo kidney transplant recipients is testing whether adding fingolimod (FTY720) to standard immunosuppression prevents expansion of the interstitial compartment of the transplanted kidney, a precursor to interstitial fibrosis and graft loss. The stated hypothesis is that abrogating the fibrogenic effects of both the RhoA and mTOR pathways with fingolimod will reduce structural damage in transplanted kidneys and possible subsequent transplant failure [4]. This is a registered trial protocol; no outcome data are reported in the evidence available here.

lncRNA DANCR and osteogenic differentiation of bone marrow mesenchymal stem cells

Work on long non-coding RNA DANCR in the context of osteoporosis investigated its role in osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) and the underlying mechanism, using sh-DANCR intervention in BMSCs. The reported mechanism involves targeting of the miR-19a-3p/PTEN/AKT/mTOR pathway [5]. This is a cell-based mechanistic study.

Anlotinib and c-MET/AKT/mTOR signalling in glioma cells

Because glioma cells show rapid proliferation, diffuse invasion and frequent recurrence, a study examined the direct antitumour effects of anlotinib in human glioma cells and whether those effects were associated with hepatocyte growth factor receptor (c-MET)/protein kinase signalling and altered autophagy-associated protein expression. The reported mechanism is suppression of c-MET/AKT/mTOR signalling [6]. This is an in vitro human cell study.

Pharmacological mTOR activation and trophectoderm differentiation in bovine embryos

Blastocyst formation is a highly orchestrated process. In mice, the mTOR pathway influences the Hippo pathway and thereby expression of trophectoderm (TE)-related genes, but these mechanisms are not fully characterised in bovine embryos. A study testing pharmacological mTOR pathway activation in bovine embryos reported that activation did not enhance trophectoderm differentiation [7]. This is an embryo model study; the finding is a negative result for the specific intervention tested.

Mitochondria-enriched BMSC exosomes and microglia-neuron cross-talk in Parkinson's disease models

Mitochondrial dysfunction and neuroinflammation drive dopaminergic neuron loss in Parkinson's disease (PD). BMSC-derived small extracellular vesicles (BMSC-Exo) are neuroprotective, but their capacity to repair mitochondrial deficits is limited; mitochondria-enriched sEVs (Exo-Mito) were therefore engineered and tested. The reported mechanism involves PINK1/parkin and PI3K/Akt/mTOR pathways in restoring microglia-neuron cross-talk [8]. This is a preclinical engineered-vesicle study.

Pathway arms referenced across the studies above

Study subject	Pathway arm named	Model
LL-37	PTEN/AKT/mTOR	Osteosarcoma cell lines and hBMSCs (in vitro)
Intramuscular fat deposition	PPAR, PI3K-Akt, mTOR	Yanbian yellow cattle (n = 60)
Alpha ketoglutarate	Inflammation (geroprotector context)	Registered CRC surgery trial protocol
Fingolimod	RhoA and mTOR	Registered kidney transplant trial protocol
lncRNA DANCR	miR-19a-3p/PTEN/AKT/mTOR	BMSCs (cell-based)
Anlotinib	c-MET/AKT/mTOR	Human glioma cells (in vitro)
mTOR activation	mTOR (Hippo interaction)	Bovine embryos
Exo-Mito	PINK1/parkin and PI3K/Akt/mTOR	PD model, engineered sEVs

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