AMPK serves as a regulator of metabolic homeostasis to conserve energy in tumor cells by inhibiting ATP-anabolic processes and promoting ATP-generating pathways. When activated, AMPK reprograms cellular metabolism and imposes growth checkpoints, particularly through inhibition of the mTOR signaling pathway. Since mTOR is activated in a subset of PanNET patients, the AMPK-mTOR signaling axis is a crucial target to evaluate the risk for chemotherapy drugs resistance and overall prognosis in these patients.
We now report that elevated TYMS levels downregulates AMPK signaling and activates mTOR signaling in PanNET tumor cells. These data suggest a new role for TYMS inhibition to modulate the AMPK-mTOR signaling axis and impact the efficacy of current mTOR inhibitory agents in the management of patients with advanced PanNET.
[doi:10.25345/C5901ZT4Z]
[dataset license: CC0 1.0 Universal (CC0 1.0)]
Keywords: TYMS, AMPK-mTOR signaling, pancreatic neuroendocrine tumors, TMT ; DatasetType:Proteomics
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Principal Investigators: (in alphabetical order) |
Maria Zajac-Kaye, University of Florida, United States |
| Submitting User: | jinkoh |
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