ArticleMedComm2025
The SUMOylated RREB1 interacts with KDM1A to induce 5-fluorouracil resistance via upregulating thymidylate synthase and activating DNA damage response pathway in colorectal cancer.
Article in MedComm, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Targeting ATF4 overcomes dual resistance to chemo-immunotherapy in gastric cancer by disrupting the DNA damage response.Journal for immunotherapy of cancer · 2026Article
- NIBAN2/FLII/RREB1 Axis Drives Glioma Stem Cell Malignancy via TLR3 Pathway Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Everolimus destabilizes thymidylate synthase via suppressing its O-GlcNAcylation and sensitizes HER2-negative breast cancer to fluorouracil.Cell death & disease · 2026Article
- Multifaceted anticancer mechanisms of tribenzyltin carboxylates: DNA minor groove targeting and inhibition of key enzymes in DNA replication, nucleotide synthesis, and redox homeostasis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- RUNX1/SLAMF3 Axis Drives Immunosuppression to Contribute to Colorectal Cancer Liver Metastasis by Blocking Phagocytosis and Depleting C1QCAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
11 authors.
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Abstract
Chemoresistance is one main cause of failure in colorectal cancer (CRC) treatment. The role of transcription factor Ras-responsive element binding protein 1 (RREB1) remains unclarified in CRC chemoresistance. Herein, we reveal that RREB1 functions as an oncogene to promote cell proliferation and 5-fluorouracil (5-FU) chemoresistance in CRC, and SUMOylation is required for RREB1 to exert its oncogenic role in CRC. RREB1 induced cell cycle arrest at the S-phase and a decreased apoptosis rate under 5-FU exposure. Mechanistically, the interaction of RREB1 with lysine demethylase 1A (KDM1A) elevated expression of 5-FU targeting proteins thymidylate synthase (TS) and thymidine kinase (TK1) to maintain the nucleotide pool balance under 5-FU treatment, and enhanced activation of Chk1-mediated DNA damage response (DDR) pathway. The deSUMOylation of RREB1 resulted in a reduced interaction of RREB1 with KDM1A, contributing to a downregulation of TS expression and a less activation of DDR pathway. Moreover, KDM1A knockdown improved the DNA damage and reduced RREB1-mediated resistance to 5-FU. These findings provide new insights into RREB1-mediated chemotherapy responses in CRC and indicate RREB1 is a potential target for overcoming 5-FU resistance.
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