FZD6 promotes 5-fluorouracil resistance through inhibiting pyroptosis in colorectal cancer

Carcinogenesis. 2025 Sep 4;46(3):bgaf041. doi: 10.1093/carcin/bgaf041.

Abstract

Resistance to 5-fluorouracil (5-FU) causes treatment failure in most colorectal cancer (CRC) cases. Pyroptosis is associated with chemotherapy resistance, although its role in 5-FU resistance in CRC is not well understood. To investigate this, we performed proteomic sequencing and bioinformatics analysis on wild-type and 5-FU-resistant CRC cell lines. Subsequently, Frizzled receptor 6 (FZD6) knockdown and overexpression cell lines were established using a lentiviral system. CCK-8, colony formation, and EdU assays were performed to assess the viability and proliferative potential of 5-FU-treated cells. The morphological changes associated with pyroptosis were examined by microscopic imaging and electron microscopy. The nuclear expression of β-catenin was examined by immunofluorescence and western blotting. These findings indicated that FZD6 protein was upregulated in the 5-FU-resistant CRC cells compared with the corresponding wild-type cell lines, an observation further validated through immunohistochemical analysis of clinical samples. Additionally, 5-FU treatment induced NLRP3/caspase-1/GSDMD-mediated classical pyroptosis in the wild-type CRC cells and decreased their viability, while the pyroptosis inhibitor Ac-FITD-CMK enhanced drug resistance. Furthermore, overexpression of FZD6 promoted nuclear translocation of β-catenin, reduced pyroptosis, and increased 5-FU resistance. In contrast, 5-FU treatment did not induce significant pyroptosis in drug-resistant cells, while pyroptosis inducers (nigericin or LPS + ATP) significantly reduced cell viability regardless of 5-FU. Moreover, knockdown of FZD6 decreased nuclear translocation of β-catenin, enhanced pyroptosis, and reduced 5-FU resistance. Finally, β-catenin knockdown enhanced pyroptosis and decreased 5-FU resistance. Thus, FZD6 promotes 5-FU resistance in CRC cells by inhibiting pyroptosis through increased nuclear translocation of β-catenin.

Keywords: FZD6; colorectal cancer; pyroptosis; resistance; β-catenin.

Plain language summary

This study provides the first evidence that FZD6 regulates 5-FU resistance via the classical pyroptosis pathway. FZD6 promotes β-catenin nuclear expression, downregulates NLRP3 levels, and inhibits the caspase-1/GSDMD pyroptosis pathway, thereby promoting 5-FU resistance.

MeSH terms

  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Colorectal Neoplasms* / drug therapy
  • Colorectal Neoplasms* / genetics
  • Colorectal Neoplasms* / metabolism
  • Colorectal Neoplasms* / pathology
  • Drug Resistance, Neoplasm* / genetics
  • Fluorouracil* / pharmacology
  • Fluorouracil* / therapeutic use
  • Frizzled Receptors* / genetics
  • Frizzled Receptors* / metabolism
  • Gene Expression Regulation, Neoplastic / drug effects
  • Humans
  • NLR Family, Pyrin Domain-Containing 3 Protein / metabolism
  • Pyroptosis* / drug effects
  • beta Catenin / metabolism

Substances

  • Fluorouracil
  • Frizzled Receptors
  • FZD6 protein, human
  • beta Catenin
  • NLR Family, Pyrin Domain-Containing 3 Protein
  • NLRP3 protein, human