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<p>Immunotherapy have led to clinical remissions in many solid tumors. However, the efficacy of immunotherapeutic monotherapy in triple-negative breast cancer (TNBC) is not very satisfactory. NSUN2 functions as a proto-oncogene in various cancers, promoting tumor cell proliferation, invasion, and metastasis. However, its role in modulating the tumor immune microenvironment, particularly in TNBC immunotherapy and its relationship with treatment sensitivity in TNBC remain to be further explored. In this study, we found that NSUN2 was highly expressed in pan-cancer, and elevated levels correlate with poor prognosis in TNBC. Furthermore, NSUN2 expression demonstrated a positive correlation with immune cell infiltration and the expression of immune checkpoint molecules. Up-regulated NSUN2 expression lowers the sensitivity of many chemotherapy drugs, and higher the sensitivity of many molecular-targeted agents. Functionally, depleted NSUN2 inhibits the proliferation and migration of TNBC cells significantly. Our study reveals the critical role of NSUN2 in regulating the immune microenvironment of TNBC, provides a theoretical foundation for its potential as a novel immunotherapy target, addresses the knowledge gap regarding NSUN2’s immunoregulatory mechanisms in TNBC, and demonstrates significant clinical translational potential.</p>

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Oncogenic and immunological roles of NSUN2 in triple negative breast cancer

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年1月6日

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  • Ning An,
  • Yi-Fan Zeng,
  • Zhuo-wan Tian,
  • Jie Tian,
  • Ling-Feng Xu,
  • Ya-Long Yang,
  • Hong-Mei Zheng,
  • Jing-Wei Zhang,
  • Yi-qing Xi

摘要

Immunotherapy have led to clinical remissions in many solid tumors. However, the efficacy of immunotherapeutic monotherapy in triple-negative breast cancer (TNBC) is not very satisfactory. NSUN2 functions as a proto-oncogene in various cancers, promoting tumor cell proliferation, invasion, and metastasis. However, its role in modulating the tumor immune microenvironment, particularly in TNBC immunotherapy and its relationship with treatment sensitivity in TNBC remain to be further explored. In this study, we found that NSUN2 was highly expressed in pan-cancer, and elevated levels correlate with poor prognosis in TNBC. Furthermore, NSUN2 expression demonstrated a positive correlation with immune cell infiltration and the expression of immune checkpoint molecules. Up-regulated NSUN2 expression lowers the sensitivity of many chemotherapy drugs, and higher the sensitivity of many molecular-targeted agents. Functionally, depleted NSUN2 inhibits the proliferation and migration of TNBC cells significantly. Our study reveals the critical role of NSUN2 in regulating the immune microenvironment of TNBC, provides a theoretical foundation for its potential as a novel immunotherapy target, addresses the knowledge gap regarding NSUN2’s immunoregulatory mechanisms in TNBC, and demonstrates significant clinical translational potential.