Nat Commun:5-FU activates the WNT/β-catenin path, promoting the dryness of colorectal cancer.

Colorectal cancer (CRC) is one of the most common cancers in the world.
fluorinated similar to urine 5-fluorouracil (5-FU) is the basic component of CRC's palliative and complementary chemotherapy drugs.
, however, the clinical benefits of 5-FU treatment are often short-lived, and most treated patients do not achieve the complete eradication of tumor cells, leading to a recurrence of 5-FU treatment leading to adverse consequences.
5-FU-based therapies, such as FOLFOX (5-FU, leprosyrin and O'Sullivan) or FOLFIRI (5-FU, leprosyrin and irithylcon), have been used as standard therapies for late CRC5.
the objective response rate of CRC patients was increased to 40-50% by 5-FU-based treatment, the disease-free life of CRC patients was not effectively extended.
therefore, strategies to improve the clinical effectiveness of 5-FU therapy are urgently needed, and understanding the mechanisms for 5-FU treatment of CRC patient recurrence is an important step in improving the survival benefits of 5-FU-based CRC therapy.
recently, researchers published a paper in the journal Nature Communications demonstrating that p53 promotes WNT3 transcription, leading to the activation of the WNT/β-catenin pathfound in ApcMin/Lgr5EGFP mice, CRC patient-origin tumor organs (PDTOs) and patient-origin tumor cells (PDCs).
this regulation, 5-FU induces the activation and abundance of cancer stem cells (CSCs) in residual tumors, which can help with post-treatment recurrence.
combination of WNT inhibitors and 5-FU effectively inhibited CSCs and reduced tumor growth after discontinuation of treatment.
The results of these studies suggest that p53 is a key medium for 5-FU to induce CSC activation through the WNT/β-catenin signaling pathrapy, and highlight the significance of WNT inhibitors and 5-FU combination therapy, which is a compelling treatment strategy that can improve the current adverse outcomes of 5-FU-based therapies in CRC patients.