Influence of pharmacological AMPK activation on Nrf2- hyperactive lung cancer cells (A549 cell line)
Description
Data originate from assessment of viability, migration, gene expression, knockdown and overexpression approaches as well as determination of ROS, NAD+ and NADH levels in metformin-treated A549 cells (including optimization experiments). They are connected with the study starting with the hypothesis (based on previous data) that AMPK activation by metformin would lead to phosphorylation and degradation of NRF2 in the KEAP-deficient background of A549 lung cancer cells and blunt the hyperactive protective shield of NRF2. Checking NRF2 half -life, regulated target genes and sensitvity to taxol and cisplatin in A549 cells showed no influence of metformin. But metformin reduced migration and BACH1 levels of A549 cells. Testing for an AMPK /BACH1/motility axis showed that metformin blunts migration in an AMPK and BACH1 independent manner. Metformin leads to reduced relative NAD+ levels which is causally involved in reduced migration as supplementation with NMN can restore motility in metformin treated cells. Most data is published open access in doi: 10.1038/s41598-026-61444-3.
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Institutions
- University of ViennaVienna, Vienna