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<p>Long non-coding RNAs (lncRNAs) are increasingly recognized as key modulators of gene expression and cellular processes, playing pivotal roles in cancer biology. In breast cancer, a multifaceted malignancy driven by diverse genetic and epigenetic alterations, the mitogen-activated protein kinase (MAPK) signaling pathway is critical for regulating processes such as cell proliferation, survival, and metastasis. Emerging research highlights intricate interactions between lncRNAs and MAPK signaling components, including ERK, p38, and JNK, revealing novel regulatory mechanisms underlying breast cancer development and progression. These interactions often involve lncRNAs modulating MAPK pathway activity or engaging in crosstalk with other oncogenic networks. This review explores how lncRNAs influence MAPK signaling in breast cancer pathogenesis, emphasizing their dual roles as potential oncogenes or tumor suppressors depending on the molecular context. While these findings suggest that lncRNAs could serve as diagnostic biomarkers or therapeutic targets to influence tumor growth, metastasis, and drug resistance, challenges such as study heterogeneity, conflicting functional outcomes, and the complexity of lncRNA-MAPK interactions limit immediate clinical translation. By elucidating these molecular relationships, we aim to provide insights into breast cancer biology and highlight the potential, as well as the limitations, of leveraging lncRNA-MAPK interactions for improved diagnostic and therapeutic strategies, pending further mechanistic and clinical validation.</p> Graphical abstract <p></p>

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Interactions between LncRNAs and MAPK signaling pathways in the pathogenesis of breast cancer

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年10月6日

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  • Baifang Ding,
  • Xuguang Wang,
  • Zhong Zhang,
  • Yiwei Wang,
  • Wei Bo,
  • Mengyuan Zhang,
  • Zitong Tian,
  • Yaolu Wang,
  • Xinyao Xue,
  • Min Zhang

摘要

Long non-coding RNAs (lncRNAs) are increasingly recognized as key modulators of gene expression and cellular processes, playing pivotal roles in cancer biology. In breast cancer, a multifaceted malignancy driven by diverse genetic and epigenetic alterations, the mitogen-activated protein kinase (MAPK) signaling pathway is critical for regulating processes such as cell proliferation, survival, and metastasis. Emerging research highlights intricate interactions between lncRNAs and MAPK signaling components, including ERK, p38, and JNK, revealing novel regulatory mechanisms underlying breast cancer development and progression. These interactions often involve lncRNAs modulating MAPK pathway activity or engaging in crosstalk with other oncogenic networks. This review explores how lncRNAs influence MAPK signaling in breast cancer pathogenesis, emphasizing their dual roles as potential oncogenes or tumor suppressors depending on the molecular context. While these findings suggest that lncRNAs could serve as diagnostic biomarkers or therapeutic targets to influence tumor growth, metastasis, and drug resistance, challenges such as study heterogeneity, conflicting functional outcomes, and the complexity of lncRNA-MAPK interactions limit immediate clinical translation. By elucidating these molecular relationships, we aim to provide insights into breast cancer biology and highlight the potential, as well as the limitations, of leveraging lncRNA-MAPK interactions for improved diagnostic and therapeutic strategies, pending further mechanistic and clinical validation.

Graphical abstract