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Background <p>Triple-negative breast cancer (TNBC) is a notoriously aggressive subtype with poor prognosis. MicroRNAs (miRNAs) critically regulate epithelial-mesenchymal transition (EMT), a central driver of cancer metastasis. Nevertheless, the function of hsa-miR-5100 in TNBC was poorly understood. This study investigated the effects of miR-5100 on the malignant behaviors of TNBC cells, its correlation with patient prognosis, and underlying molecular mechanisms.</p> Methods <p>Plasma levels of miR-5100 were assessed in a cohort of 80 TNBC patients and 80 healthy controls. Based on miR-5100 expression levels, patients were categorized into high and low groups, with 5-year survival as the primary endpoint for Kaplan-Meier and Cox regression analyses. MiR-5100 was assessed for its effects on proliferation, migration, invasion, and EMT in TNBC cell lines (MDA-MB-231 and MDA-MB-468), with its direct interaction with SMAD4 confirmed by dual-luciferase reporter assay.</p> Results <p>Upregulation of miR-5100 was observed in TNBC patients. Elevated miR-5100 levels correlated with advanced TNM stage, lymph node metastasis, high Ki-67 proliferation index, and reduced survival. Overexpression of miR-5100 promoted the proliferation, migration and invasion of TNBC cells. MiR-5100 overexpression mediated the reciprocal regulation of E-cadherin (down) and N-cadherin (up) at both mRNA and protein levels in TNBC cells. Mechanistically, the oncogenic effects of miR-5100 on TNBC cell proliferation, migration, invasion, and EMT were mediated through its direct targeting of SMAD4.</p> Conclusions <p>MiR-5100 was upregulated in TNBC patients and was associated with a poor prognosis. By targeting SMAD4, miR-5100 promoted the malignant phenotypes of TNBC cells in vitro, suggesting its potential research value as a prognostic biomarker and therapeutic target.</p>

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MiR-5100 promotes the malignant phenotype of triple-negative breast cancer cells by targeting SMAD4 and predicts poor prognosis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月28日

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  • Yaxi Song,
  • Haiyan Wei,
  • Jing Zhai,
  • Peng Dai,
  • Lei Han

摘要

Background

Triple-negative breast cancer (TNBC) is a notoriously aggressive subtype with poor prognosis. MicroRNAs (miRNAs) critically regulate epithelial-mesenchymal transition (EMT), a central driver of cancer metastasis. Nevertheless, the function of hsa-miR-5100 in TNBC was poorly understood. This study investigated the effects of miR-5100 on the malignant behaviors of TNBC cells, its correlation with patient prognosis, and underlying molecular mechanisms.

Methods

Plasma levels of miR-5100 were assessed in a cohort of 80 TNBC patients and 80 healthy controls. Based on miR-5100 expression levels, patients were categorized into high and low groups, with 5-year survival as the primary endpoint for Kaplan-Meier and Cox regression analyses. MiR-5100 was assessed for its effects on proliferation, migration, invasion, and EMT in TNBC cell lines (MDA-MB-231 and MDA-MB-468), with its direct interaction with SMAD4 confirmed by dual-luciferase reporter assay.

Results

Upregulation of miR-5100 was observed in TNBC patients. Elevated miR-5100 levels correlated with advanced TNM stage, lymph node metastasis, high Ki-67 proliferation index, and reduced survival. Overexpression of miR-5100 promoted the proliferation, migration and invasion of TNBC cells. MiR-5100 overexpression mediated the reciprocal regulation of E-cadherin (down) and N-cadherin (up) at both mRNA and protein levels in TNBC cells. Mechanistically, the oncogenic effects of miR-5100 on TNBC cell proliferation, migration, invasion, and EMT were mediated through its direct targeting of SMAD4.

Conclusions

MiR-5100 was upregulated in TNBC patients and was associated with a poor prognosis. By targeting SMAD4, miR-5100 promoted the malignant phenotypes of TNBC cells in vitro, suggesting its potential research value as a prognostic biomarker and therapeutic target.