PFKFB3-dependent redox homeostasis and DNA repair support cell survival under EGFR-TKIs in non-small cell lung carcinoma
Our results suggest that PFKFB3 inhibition reduces glucose utilization and DNA damage repair, limiting the adaptivity of the cells to therapy-driven oxidative stress and DNA integrity insults. Inhibiting PFKFB3 can be an effective strategy to eradicate cancer cells surviving under EGFR TKI therapy before they enter the drug-resistant state. These findings may have potential implications in the development of new therapies for drug-resistant cancer treatment.
Authors
- Xinmin Yin (ORCID: https://orcid.org/0000-0001-5716-3458)
- Brian F. Clem (ORCID: https://orcid.org/0000-0002-9082-8914)
- Susan Dougherty
- Nadiia Lypova (ORCID: https://orcid.org/0000-0003-1506-8545)
- Yoannis Imbert-Fernandez (ORCID: https://orcid.org/0000-0003-1474-3027)
- Jason Chesney (ORCID: https://orcid.org/0000-0003-0217-8278)
- Xiang Zhang (ORCID: https://orcid.org/0000-0003-1102-6313)
- Xiaohong Li (ORCID: https://orcid.org/0000-0001-8345-9164)
- Jing Feng (ORCID: https://orcid.org/0000-0003-0242-3114)
Institutions
- University of Louisville (US)
Publication Details
- Journal
- Cancer & Metabolism
- Published
- 2024-12-18
- DOI
- https://doi.org/10.1186/s40170-024-00366-y
- Citations
- 4
- Primary Topic
- DNA Repair Mechanisms
- Type
- article
- Field-Weighted Citation Impact
- 0.94