ArticleOncogene2022
Non-genomic activation of the AKT-mTOR pathway by the mitochondrial stress response in thyroid cancer.
Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Glucose Metabolic Reprogramming in Thyroid Cancer: Underlying Molecular Mechanisms and Links to Progression and Treatment.Current medical science · 2026Review
- Development of a prognostic model for thyroid cancer based on mitochondrial metabolism-related genes and immune profiling.World journal of surgical oncology · 2026Article
- The Role of Mitochondrial Genome Stability and Metabolic Plasticity in Thyroid Cancer.Biomedicines · 2025Review
- Ganoderic acid a derivative induces apoptosis of cervical cancer cells by inhibiting JNK pathway.Chinese herbal medicines · 2025Article
- Radiotranscriptomics in papillary thyroid carcinoma complement current noninvasive risk stratification system.Science advances · 2025Article
- Metabolic Reprogramming in Thyroid Cancer.Endocrinology and metabolism (Seoul, Korea) · 2024Review
- SIRT3 enhances the protective effect of Xyloketal B on seizure-induced brain injury by regulating AMPK/mTOR signaling-mediated autophagy.The Kaohsiung journal of medical sciences · 2024Article
- Lysosomes mediate the mitochondrial UPR via mTORC1-dependent ATF4 phosphorylation.Cell discovery · 2023Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer progression is associated with metabolic reprogramming and causes significant intracellular stress; however, the mechanisms that link cellular stress and growth signalling are not fully understood. Here, we identified a mechanism that couples the mitochondrial stress response (MSR) with tumour progression. We demonstrated that the MSR is activated in a significant proportion of human thyroid cancers via the upregulation of heat shock protein D family members and the mitokine, growth differentiation factor 15. Our study also revealed that MSR triggered AKT/S6K signalling by activating mTORC2 via activating transcription factor 4/sestrin 2 activation whilst promoting leucine transporter and nutrient-induced mTORC1 activation. Importantly, we found that an increase in
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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.