Cysteine Depletion-Initiated Redox Imbalance Evokes Ferroptosis and Pyroptosis for Enhanced Pancreatic Cancer Therapy
Source abstract
Abstract
Highly proliferative and reactive oxygen species (ROS) overexpression make pancreatic cancer upregulate cysteine (Cys) uptake to maintain redox homeostasis, which indicates that Cys may be a potential target for the treatment of pancreatic cancer. Herein, polyvinylpyrrolidone (PVP) modified CuO nanoparticles ( PVP CuO NPs) are proposed first for inducing redox imbalance initiated by cysteine (Cys) depletion. The PVP CuO NPs not only deplete cysteine and produce H 2 O 2 but also exhibit peroxidase (POD)-like activity, efficiently converting H 2 O 2 into hydroxyl radicals ( • OH). Simultaneously, Cys depletion also induces nicotinamide adenine dinucleotide phosphate (NADPH) consumption and thioredoxin (TXN) synthesis to trigger ferroptosis. Then the remarkable redox imbalance together with a mass of Cu 2+ ions generation further initiate pyroptosis, achieving Cys targeted high-efficiency pancreatic cancer therapy.
Source: openalex_inverted_index · Quality: baseline
Research context
OpenAlex topics: Nanoplatforms for cancer theranostics · Advanced Nanomaterials in Catalysis · Metal-Organic Frameworks: Synthesis and Applications
SciVX discovery tags are terminology-based. OpenAlex topics are source-provided classifications.
Affiliations
State Key Laboratory of Rare Earth Resource Utilization, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences, Changchun 130022, China
School of Applied Chemistry and Engineering, University of Science and Technology of China, Hefei 230026, China
Funding
National Key Research and Development Program of China · Jilin Provincial Scientific and Technological Development Program · National Natural Science Foundation of China
References (36)
Show source-provided references
1. 10.1001/jama.2019.1023210.1001/jama.2019.10232 ↗
2. 10.1038/nature1018910.1038/nature10189 ↗
3. 10.1074/jbc.M50643920010.1074/jbc.M506439200 ↗
4. 10.1016/j.cbi.2005.12.00910.1016/j.cbi.2005.12.009 ↗
5. 10.1016/j.cellsig.2012.01.00810.1016/j.cellsig.2012.01.008 ↗
6. 10.1016/j.ajps.2021.10.00310.1016/j.ajps.2021.10.003 ↗
7. 10.1016/j.ajps.2022.07.00610.1016/j.ajps.2022.07.006 ↗
8. 10.1016/j.nantod.2022.10166310.1016/j.nantod.2022.101663 ↗
9. 10.1002/adma.20230593210.1002/adma.202305932 ↗
10. 10.1002/adhm.20220336210.1002/adhm.202203362 ↗
11. 10.1021/acsnano.3c0136910.1021/acsnano.3c01369 ↗
12. 10.1002/VIW.2020014710.1002/VIW.20200147 ↗
13. 10.1073/pnas.181493211610.1073/pnas.1814932116 ↗
14. 10.1016/S1535-6108(04)00117-510.1016/S1535-6108(04)00117-5 ↗
15. 10.1126/science.aaw987210.1126/science.aaw9872 ↗
16. 10.1023/A:102100932284310.1023/A:1021009322843 ↗
17. 10.1002/smll.20220270510.1002/smll.202202705 ↗
18. 10.1016/j.biomaterials.2023.12230010.1016/j.biomaterials.2023.122300 ↗
19. 10.1002/anie.20221017410.1002/anie.202210174 ↗
20. 10.1038/s41586-019-1170-y10.1038/s41586-019-1170-y ↗
21. 10.1016/j.cell.2012.03.04210.1016/j.cell.2012.03.042 ↗
22. 10.1016/j.nantod.2021.10115010.1016/j.nantod.2021.101150 ↗
23. 10.1016/j.chembiol.2019.01.00810.1016/j.chembiol.2019.01.008 ↗
24. 10.1002/INMD.2022000510.1002/INMD.20220005 ↗
25. 10.1016/j.jcrysgro.2006.06.03810.1016/j.jcrysgro.2006.06.038 ↗
26. 10.1002/asia.20130133310.1002/asia.201301333 ↗
27. 10.1039/C6RA08359E10.1039/C6RA08359E ↗
28. 10.1016/j.bios.2017.05.03710.1016/j.bios.2017.05.037 ↗
29. 10.1246/bcsj.56.206510.1246/bcsj.56.2065 ↗
30. 10.1007/s13238-020-00789-510.1007/s13238-020-00789-5 ↗
31. 10.1002/adma.20190405810.1002/adma.201904058 ↗
32. 10.1016/j.cmet.2019.01.02010.1016/j.cmet.2019.01.020 ↗
33. 10.1002/anie.20221530710.1002/anie.202215307 ↗
34. 10.1002/ange.20230770610.1002/ange.202307706 ↗
35. 10.1038/cr.2016.10010.1038/cr.2016.100 ↗
36. 10.1016/j.chom.2018.05.00910.1016/j.chom.2018.05.009 ↗