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Related Concept Videos

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The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which...
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Related Experiment Video

Updated: Apr 17, 2026

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RUNX1 Directly Activates WNT2 to Orchestrate Tumor-Associated Macrophage Reprogramming in Colorectal Cancer.

Wei Sun1, Xiaohui Ren2, Shuqing Wei1

  • 1Department of General Medicine, Shanxi Province Cancer Hospital, Shanxi Hospital Affiliated to Cancer Hospital, Chinese Academy of Medical Sciences, Cancer Hospital Affiliated to Shanxi Medical University, Taiyuan, China.

Molecular Carcinogenesis
|April 15, 2026
PubMed
Summary

The RUNX1-WNT2 axis drives colorectal cancer (CRC) progression by promoting M2 macrophage polarization and metastasis. Targeting this axis offers a potential therapeutic strategy for CRC.

Keywords:
RUNX1WNT2colorectal cancermacrophagestumor microenvironment (TME)

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Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Tumor-associated macrophages (TAMs), especially M2 subtype, promote immune suppression and metastasis in colorectal cancer (CRC).
  • WNT2 is upregulated in cancers, and RUNX1 is an oncogenic factor, but their axis in CRC progression and M2 polarization was unclear.

Purpose of the Study:

  • To investigate the role of a RUNX1-WNT2 axis in M2 macrophage polarization and colorectal cancer progression.
  • To elucidate the regulatory mechanism of RUNX1 on WNT2 and the functional impact of this axis on CRC growth and metastasis.

Main Methods:

  • Expression profiling (GEPIA, TCGA), quantitative RT-PCR, Western blotting, immunohistochemistry in CRC tissues.
  • In vitro assays (CCK-8, colony formation, Transwell) in CRC cell lines, co-culture with THP-1 macrophages for polarization analysis (flow cytometry, ELISA).
  • ChIP-qPCR, dual-luciferase reporter assays for RUNX1-WNT2 interaction; in vivo xenograft and metastasis models with rescue studies (antibody, inhibitor).

Main Results:

  • WNT2 was overexpressed in CRC and correlated with M2-TAM signatures. WNT2 knockdown inhibited CRC cell viability, migration, invasion, and shifted M2 macrophages to M1 phenotype.
  • RUNX1 directly activated WNT2 transcription. RUNX1 knockdown decreased WNT2 expression, while overexpression increased it.
  • In vivo, WNT2 silencing reduced tumor growth, metastasis, and altered macrophage polarization. Blocking M2 polarization or macrophage depletion mitigated WNT2-driven tumor progression.

Conclusions:

  • RUNX1 directly activates WNT2, promoting cytokine production and M2 macrophage polarization, which accelerates CRC growth and metastasis.
  • The RUNX1-WNT2 axis represents a potential therapeutic target and biomarker framework for colorectal cancer treatment.