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Background <p>MicroRNAs (miRNAs) are short non-coding RNAs that regulate gene expression post-transcriptionally. miR-122 is abnormally expressed in breast cancer, functioning as both a tumor suppressor and oncomiR, however, its role in triple-negative breast cancer (TNBC) remains unclear.</p> Purpose <p>In this study we investigate the molecular mechanism of miR-122 in TNBC patients undergoing neoadjuvant chemotherapy (NAC).</p> Methods <p>We analyzed the expression of miR-122 and its clinical association in TNBC patients from TCGA and KM-plotter datasets. Functional analysis was performed by modulating miR-122 levels in TNBC cells through antagomiR transfections for knockdown assays, and mimic-miR-122 assays, followed by RT-qPCR, immunoblotting, cell viability and migration assays.</p> Results <p>Downregulation of miR-122 in TNBC patients is associated with tumor recurrence but not with pathologic complete response after NAC. Low miR-122 levels in rapid-relapse TNBC patients activate a gene co-expression network enriched in genes linked to migration, invasion, and cell differentiation. Among these, DNA-binding protein BORIS was identified as a target of miR-122. Overexpression of miR-122 inhibited cell migration and BORIS expression. Additionally, BORIS promoted a gene expression profile related to cell differentiation and cytoskeletal components in TNBC tumors deficient of miR-122.</p> Conclusion <p>The loss of miR-122 in TNBC tumors is associated with rapid relapse after chemotherapy in patients and allows cell migration by promoting a metastatic-related transcriptomic landscape, including positive modulation of BORIS expression.</p>

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Loss of miR-122 promotes cell migration and poor prognosis in triple-negative breast cancer treated by neoadjuvant chemotherapy

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月22日

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  • Mauricio Flores-Fortis,
  • Isidro X. Perez-Añorve,
  • Carlos C. Patiño-Morales,
  • Ernesto Soto-Reyes,
  • Claudia H. Gonzalez-De la Rosa,
  • Joaquin Manzo-Merino,
  • Arturo Aguilar-Rojas,
  • Nicolas Villegas,
  • Elena Arechaga-Ocampo

摘要

Background

MicroRNAs (miRNAs) are short non-coding RNAs that regulate gene expression post-transcriptionally. miR-122 is abnormally expressed in breast cancer, functioning as both a tumor suppressor and oncomiR, however, its role in triple-negative breast cancer (TNBC) remains unclear.

Purpose

In this study we investigate the molecular mechanism of miR-122 in TNBC patients undergoing neoadjuvant chemotherapy (NAC).

Methods

We analyzed the expression of miR-122 and its clinical association in TNBC patients from TCGA and KM-plotter datasets. Functional analysis was performed by modulating miR-122 levels in TNBC cells through antagomiR transfections for knockdown assays, and mimic-miR-122 assays, followed by RT-qPCR, immunoblotting, cell viability and migration assays.

Results

Downregulation of miR-122 in TNBC patients is associated with tumor recurrence but not with pathologic complete response after NAC. Low miR-122 levels in rapid-relapse TNBC patients activate a gene co-expression network enriched in genes linked to migration, invasion, and cell differentiation. Among these, DNA-binding protein BORIS was identified as a target of miR-122. Overexpression of miR-122 inhibited cell migration and BORIS expression. Additionally, BORIS promoted a gene expression profile related to cell differentiation and cytoskeletal components in TNBC tumors deficient of miR-122.

Conclusion

The loss of miR-122 in TNBC tumors is associated with rapid relapse after chemotherapy in patients and allows cell migration by promoting a metastatic-related transcriptomic landscape, including positive modulation of BORIS expression.