Supplementary Figure 8 from USP15 Facilitates Colorectal Cancer Immune Evasion through SMYD3/CCL2-Dependent Myeloid-Derived Suppressor Cell Recruitment

Shuling Han; Luying Cui; Bojun Wang; Yuli Ruan; Mengde Shi; Chang Hong; Xin Guan; Zhuo Chen; Yingjue Li; Yuanyu Liao; Ming Ma; Xiaolin Lu; Andi Wang; Yanqiao Zhang; Chao Liu

doi:10.1158/2326-6066.29760247

August 1, 2025

Supplementary Figure 8 from USP15 Facilitates Colorectal Cancer Immune Evasion through SMYD3/CCL2-Dependent Myeloid-Derived Suppressor Cell Recruitment

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Key Points

MAIN FINDING: USP15 is shown to facilitate immune evasion in colorectal cancer through the recruitment of myeloid-derived suppressor cells.
KEY EVIDENCE: SMYD3 is responsible for promoting CCL2 expression, leading to enhanced recruitment of immune suppressive cells.
APPROACH: The study identifies trimethylation of H3K4 as a key mechanism by which SMYD3 enhances CCL2 expression in CRC.
SIGNIFICANCE: Understanding this mechanism may provide insights into new therapeutic targets for improving immune responses in colorectal cancer.

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Implication

Research reveals USP15 facilitates immune evasion in colorectal cancer by recruiting myeloid-derived suppressor cells, highlighting the role of SMYD3 and CCL2.

Abstract

SMYD3 promotes CCL2 expression via trimethylation of H3K4 in CRC.

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Han et al. (2025) studied this question.

synapsesocial.com/papers/689a0c72e6551bb0af8d024b https://doi.org/10.1158/2326-6066.29760247

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Supplementary Figure 8 from USP15 Facilitates Colorectal Cancer Immune Evasion through SMYD3/CCL2-Dependent Myeloid-Derived Suppressor Cell Recruitment

Key Points

No abstract yet

Implication

Abstract

Discussion

Cite This Study

Supplementary Figure 8 from USP15 Facilitates Colorectal Cancer Immune Evasion through SMYD3/CCL2-Dependent Myeloid-Derived Suppressor Cell Recruitment

Key Points

No abstract yet

Implication

Abstract

Discussion

Cite This Study

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