Authors
Chaozhu Pei, Ziwu Xu, Min Ouyang, Huitong Bu, Zhenyu Zou, Yuting Ma, Zhengqing Zhu, Yan Chen, Li Yu, Mingmin Huang, Yongjun Tan
Published in
Journal of pharmaceutical analysis. Volume 16. Issue 6. Pages 101493. Epub Nov 07, 2025.
Abstract
Multiple cancers overexpress forkhead (FOX) box M1 (FOXM1), a transcription factor (TF) that holds great promise for developing cancer drugs. Herein, through yeast-two-hybrid (Y2H) screening, we obtained a novel FOXM1-targeting peptide M1-NP1, which significantly inhibited the cell cycle and migration of cancer cells. Mechanistically, M1-NP1 bound to the C-terminal region of FOXM1 and disrupted its interactions with the cell cycle-related kinase polo-like kinase 1 (PLK1) and the transcriptional co-activator cyclic adenosine monophosphate (AMP) response element-binding protein (CREB) binding protein (CBP), thus inhibiting FOXM1 transcriptional activities. Additionally, M1-NP1 affected FOXM1 distribution in cells, preventing FOXM1 from infiltrating the nucleus to exert its effects. Furthermore, M1-NP1 treatment in cancer cells downregulated the gene sets of cell cycle phase transition and upregulated the gene sets of cell adhesion. Moreover, M1-NP1's anti-cancer effects were confirmed in wild-type (WT) mice, without any notable toxic or side effects. In addition to its good safety indications, such as the low levels of immunogenicity and hemolysis, M1-NP1 also exhibited a favorable profile regarding stability and distribution in mice. Overall, M1-NP1 targets FOXM1 for cancer therapy.
PMID:
42376477
Bibliographic data and abstract were imported from PubMed on 30 Jun 2026.
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