RUNX1-MUC13 Interaction in Wnt/β-Catenin Activation in CRC

Colorectal cancer (CRC) remains a global health challenge, often associated with metastasis and poor prognosis. RUNX1 acts as both an oncogene and tumor suppressor in several cancers, including CRC. However, its specific regulatory mechanisms in CRC are not entirely clear.

Xinyi Chen and their team aimed to investigate RUNX1’s role in CRC progression and its interaction with MUC13.

The study analyzed RUNX1 expression in CRC tissues and cell lines compared to controls. They conducted in vitro and in vivo assays to assess how RUNX1 overexpression and knockdown influence CRC cell behavior. They also used ChIP-seq and RNA-seq analyses to identify RUNX1’s target genes, focusing on MUC13.

The results demonstrated that RUNX1 expression was significantly higher in CRC tissues and correlated with advanced disease characteristics and worse patient outcomes.

Overexpressing RUNX1 increased cancer cell proliferation, migration, invasion, and G2/M phase arrest, while knockdown decreased these effects. RUNX1 was identified as a direct transcriptional regulator of MUC13, and this interaction activated the Wnt/β-catenin pathway. Disrupting MUC13 partially reversed the malignancy induced by RUNX1.

The study concluded that RUNX1 promotes CRC progression by upregulating MUC13 and activating the Wnt/β-catenin signaling pathway, identifying the RUNX1-MUC13 axis as a potential therapeutic target for managing CRC.

This research was funded by the National Natural Science Foundation of China (Grant Nos. 82130092 and 82373522) and Tongji Hospital Foundation (Grant No. 2023B27).

Source: https://pubmed.ncbi.nlm.nih.gov/39309442/

Chen X, Tu J, Yang M, et al. (2024). “RUNX1-MUC13 Interaction Activates Wnt/β-Catenin Signaling Implications for Colorectal Cancer Metastasis.” Int J Biol Sci. 2024;20(12):4999-5026. Published 2024 Sep 16. doi:10.7150/ijbs.98396