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Background <p>Pentraxin 3 (PTX3) is an inflammatory mediator involved in tumorigenesis; however, its role in tumor immune evasion remains elusive. Herein, we demonstrate that PTX3 promotes immune evasion in breast cancer by upregulating PD-L1.</p> Methods <p>RT-qPCR and Western blot were performed to assess PD-L1 expression in human and murine breast cancer cells. Cell surface PD-L1 was assayed by flow cytometry. Small interfering RNA and CRISPR-Cas9 were used to inhibit PTX3 expression. Co-culture experiments were conducted to evaluate the suppressive effects of tumor cells on CD8 + T cell activation. An immunocompetent BALB/c mouse allograft model was utilized, and tumor-infiltrating CD8 + T cells were analyzed by flow cytometry and immunohistochemistry.</p> Results <p>PTX3 enhanced PD-L1 protein levels through the inhibition of autophagy. PTX3 increased the expression of the E3 ligase RNF216 and caused Beclin-1 degradation, which suppressed autophagy, thereby preventing autophagy–mediated PD-L1 degradation. Co-culture experiments demonstrate that PTX3-overexpressing breast cancer cells suppressed CD8 + T cell function, as evidenced by reduced production of IFN-γ and Granzyme B, whereas PTX3-depleted cells had the opposite effects. In vivo allograft studies revealed that depletion of PTX3 reduced PD-L1 expression, enhanced CD8 + T cell infiltration, and inhibited tumor growth in immunocompetent mice.</p> Conclusion <p>PTX3 promotes PD-L1 expression and immune evasion in breast cancer. Therefore, targeting PTX3 may represent a potential therapeutic strategy to counteract this immune escape.</p>

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PTX3 induces the expression of PD-L1 and promotes breast cancer immune escape

  • 期刊论文

  • 发表日期：

    2026年8月3日

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  • Liyuan Jing,
  • Jie Lun,
  • Jianxin Xu,
  • Zhengyu Jin,
  • Xingqian Liu,
  • Yu Wang,
  • Yuying Zhang,
  • Min Gao,
  • Mengchao Yu,
  • Hongwei Zhang,
  • Jing Fang

摘要

Background

Pentraxin 3 (PTX3) is an inflammatory mediator involved in tumorigenesis; however, its role in tumor immune evasion remains elusive. Herein, we demonstrate that PTX3 promotes immune evasion in breast cancer by upregulating PD-L1.

Methods

RT-qPCR and Western blot were performed to assess PD-L1 expression in human and murine breast cancer cells. Cell surface PD-L1 was assayed by flow cytometry. Small interfering RNA and CRISPR-Cas9 were used to inhibit PTX3 expression. Co-culture experiments were conducted to evaluate the suppressive effects of tumor cells on CD8 + T cell activation. An immunocompetent BALB/c mouse allograft model was utilized, and tumor-infiltrating CD8 + T cells were analyzed by flow cytometry and immunohistochemistry.

Results

PTX3 enhanced PD-L1 protein levels through the inhibition of autophagy. PTX3 increased the expression of the E3 ligase RNF216 and caused Beclin-1 degradation, which suppressed autophagy, thereby preventing autophagy–mediated PD-L1 degradation. Co-culture experiments demonstrate that PTX3-overexpressing breast cancer cells suppressed CD8 + T cell function, as evidenced by reduced production of IFN-γ and Granzyme B, whereas PTX3-depleted cells had the opposite effects. In vivo allograft studies revealed that depletion of PTX3 reduced PD-L1 expression, enhanced CD8 + T cell infiltration, and inhibited tumor growth in immunocompetent mice.

Conclusion

PTX3 promotes PD-L1 expression and immune evasion in breast cancer. Therefore, targeting PTX3 may represent a potential therapeutic strategy to counteract this immune escape.