ArticleCell death & disease2025
Synergistic antitumor activity of sorafenib and the NUPR1 inhibitor LZX-2-73 in multiple cancer models.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Lipid Peroxidation in Cancer Therapy: Molecular Mechanisms Involving Oxidative Stress, Cell Death, and Therapeutic Response.Molecules (Basel, Switzerland) · 2026Review
- NUPR1 as a central stress-adaptation node in cancer: integrating metabolic rewiring, cell death, and therapy resistance.Journal of biomedical science · 2026Review
- Targeting Selectivity: Improving Golgi α-Mannosidase II (GMII) Inhibitors Through In Silico Studies.Biomolecules · 2026Review
- NUPR1 in breast cancer: mechanisms and potential applications.Frontiers in physiology · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Combination therapy in cancer treatment offers significant potential to overcome drug resistance, enhance efficacy, reduce toxicity, and expand drug indications. sorafenib, an FDA-approved multi-targeted kinase inhibitor, has demonstrated effectiveness across various cancers but currently lacks approved combination therapies. Recently, we identified LZX-2-73 as a promising drug candidate with potent anticancer activity, targeting the nuclear protein 1 (NUPR1), an emerging and promising target in cancer therapy. In this study, we report that the combination of the NUPR1 inhibitor LZX-2-73 with sorafenib produces strong synergistic anticancer effects in various cancer cell lines as well as in primary pancreatic ductal adenocarcinoma (PDAC) organoids. This combination significantly enhanced lactate dehydrogenase (LDH) release and caspase 3/7 activity, markedly induced ROS accumulation, reduced the reduced/oxidized glutathione ratio, and increased the accumulation of malondialdehyde (MDA) and lipid hydroperoxides. Collectively, the combination of LZX-2-73 and sorafenib led to a substantial increase in cell death due to massive oxidative stress. Additionally, in a pancreatic cancer xenograft mouse model, the combination of LZX-2-73 and sorafenib exhibited a synergistic anticancer effect, effectively inhibiting tumor growth. In summary, this study provides valuable insights into enhancing the anticancer activity of NUPR1 inhibitors through combination with sorafenib, offering a promising new avenue for cancer therapy and opening new indications.
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