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Background <p>Colorectal cancer (CRC) liver metastasis is a major factor affecting the prognosis of advanced CRC. Tumor-associated macrophages (TAMs), play a crucial role in CRC progression and metastasis by influencing the EMT of tumor cells. LRR binding FLII interacting protein 1, an epigenetic regulatory gene, a cancer-associated gene in a comprehensive analysis of human genome sequences; however, its role in CRC TAMs has not been elucidated.</p> Methods <p>We explored the expression and mechanism of action of LRRFIP1 in TAMs by single-cell transcriptome database analysis, immunostaining, flow cytometry, Western blotting, real-time quantitative PCR, enzyme-linked immunosorbent assay, and Transwell assay. Tumor growth and liver metastasis were examined in vivo.</p> Results <p>After knock down LRRFIP1 in TAMs in vitro, M2 phenotype and related cytokine expression were suppressed, whereas the promotion of CRC cell growth, migration, and invasion was inhibited. Interfering with LRRFIP1 did not further inhibit the TAMs phenotype or CRC progression after application of PI3K inhibitors or TGF-β receptor inhibitors.</p> Conclusions <p>LRRFIP1 induces M2-like macrophage polarization via the PI3K/AKT signaling pathway, contributing to colorectal cancer progression.</p>

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Tumor-associated macrophage-specific LRRFIP1 promotes M2 macrophage polarization and progression of colorectal cancer via activation of the PI3K pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月29日

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  • Silong Mu,
  • Shuomin Zhang,
  • Maihuan Wang,
  • Xinpu Yuan,
  • Guijun Zou,
  • Chaojun Zhang,
  • Zhen Cao

摘要

Background

Colorectal cancer (CRC) liver metastasis is a major factor affecting the prognosis of advanced CRC. Tumor-associated macrophages (TAMs), play a crucial role in CRC progression and metastasis by influencing the EMT of tumor cells. LRR binding FLII interacting protein 1, an epigenetic regulatory gene, a cancer-associated gene in a comprehensive analysis of human genome sequences; however, its role in CRC TAMs has not been elucidated.

Methods

We explored the expression and mechanism of action of LRRFIP1 in TAMs by single-cell transcriptome database analysis, immunostaining, flow cytometry, Western blotting, real-time quantitative PCR, enzyme-linked immunosorbent assay, and Transwell assay. Tumor growth and liver metastasis were examined in vivo.

Results

After knock down LRRFIP1 in TAMs in vitro, M2 phenotype and related cytokine expression were suppressed, whereas the promotion of CRC cell growth, migration, and invasion was inhibited. Interfering with LRRFIP1 did not further inhibit the TAMs phenotype or CRC progression after application of PI3K inhibitors or TGF-β receptor inhibitors.

Conclusions

LRRFIP1 induces M2-like macrophage polarization via the PI3K/AKT signaling pathway, contributing to colorectal cancer progression.