ArticleClinical and translational medicine2020
Combinational therapy targeting the MET-mTOR-ROS loop disrupts mitochondrial autoregulatory machinery of liver cancer.
Article in Clinical and translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Targeting MET and mTOR Synergistically Overcomes Adaptive Resistance in Glioblastoma.International journal of molecular sciences · 2026Article
- BNIP3-mTOR Signaling Mediates Resistance to MET Inhibition in Glioblastoma.bioRxiv : the preprint server for biology · 2025Article
- Radiomics signatures based on contrast-enhanced CT for preoperative prediction of the Ki-67 proliferation state in gastrointestinal stromal tumors.Japanese journal of radiology · 2023Article
- A novel targeted co-delivery nanosystem for enhanced ovarian cancer treatment via multidrug resistance reversion and mTOR-mediated signaling pathway.Journal of nanobiotechnology · 2021Article
- A CT-based nomogram for predicting the malignant potential of primary gastric gastrointestinal stromal tumors preoperatively.Abdominal radiology (New York) · 2021Article
- Combinational therapy targeting the MET-mTOR-ROS loop disrupts mitochondrial autoregulatory machinery of liver cancer.Clinical and translational medicine · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
A wide variety of regulators have been identified in mechanistic target of rapamycin (mTOR) activation; however, the protective mechanisms of mTOR inactivation are still largely unknown, especially in tumor growth. Here, we have found the hepatocyte growth factor (HGF) receptor (MET) is required for mTOR activation-stimulated mitochondrial oxidative phosphorylation (OXPHOS) in a phosphorylation-dependent manner in liver cancer. Intriguingly, we observed mitochondrial quality dictates the regulatory effects of MET on mTOR and OXPHOS. Once overloaded, mitochondrial reactive oxygen species (ROS) inhibits mTOR activity and OXPHOS performance to prevent mitochondrial dysfunction-induced tumor cell death, by disrupting MET dimerization to block its autophosphorylation and interaction with vacuolar ATP synthase (V-ATPase). The MET-mTOR-ROS loop acts as a protective checkpoint in liver cancer, and thus this autoregulatory machinery is a promising combinational target for liver cancer therapy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.