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Background <p>The functional mechanism of the long non-coding RNAs (lncRNA) GAPLINC in triple-negative breast cancer (TNBC) remains poorly understood. The present study aimed to explore GAPLINC in TNBC and its contribution to regulating tumor progression through the microRNA (miRNA)-331-3p/ insulin-like growth factor 2 mRNA-binding protein 1(IGF2BP1) axis.</p> Methods <p>Tumor tissue samples and adjacent normal tissue samples were collected from 150 TNBC patients, and TNBC-related cell lines were cultured. mRNA expression was determined using reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR). Functional parameters were assessed through the following experimental methods: the cell counting kit-8 (CCK-8) assay was employed to evaluate proliferation capacity, the Transwell was conducted to assess migration and invasion, and the dual-luciferase assay was performed to confirm the targeted binding relationships.</p> Results <p>GAPLINC was significantly upregulated in TNBC tissues and cell lines (<i>P</i> &lt; 0.001), and its expression was closely correlated with poor clinical prognosis. Similarly, miR-331-3p was markedly downregulated in TNBC samples (<i>P</i> &lt; 0.001), while IGF2BP1 expression was significantly overexpressed (<i>P</i> &lt; 0.001). Silencing GAPLINC effectively suppressed proliferation, migration, and invasion, accompanied by a notable upregulation miR-331-3p expression (<i>P</i> &lt; 0.001). Importantly, inhibition of miR-331-3p partially reversed the suppressive effects induced by GAPLINC knockdown. Furthermore, miR-331-3p targeted IGF2BP1. Additional knockdown of IGF2BP1 counteracted this reversal effect, thereby effectively abrogating the tumor-promoting function of GAPLINC.</p> Conclusion <p>This study identified GAPLINC as a crucial oncogenic lncRNA in TNBC. It promoted tumor progression by competitively binding to miR-331-3p, thereby derepressing its target IGF2BP1. These findings not only elucidated a new GAPLINC/miR-331-3p/IGF2BP1 regulatory axis, but also highlighted that GAPLINC may be a potential prognostic biomarker for triple-negative breast cancer.</p>

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Lnc RNA GAPLINC affects triple-negative breast cancer progression through the miR-331-3p/IGF2BP1 axis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月18日

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  • Wenyan Wang,
  • Lina Huang,
  • Siyue Zhang,
  • Ziguo Yang,
  • Shaocong Yan,
  • Guijun Yan

摘要

Background

The functional mechanism of the long non-coding RNAs (lncRNA) GAPLINC in triple-negative breast cancer (TNBC) remains poorly understood. The present study aimed to explore GAPLINC in TNBC and its contribution to regulating tumor progression through the microRNA (miRNA)-331-3p/ insulin-like growth factor 2 mRNA-binding protein 1(IGF2BP1) axis.

Methods

Tumor tissue samples and adjacent normal tissue samples were collected from 150 TNBC patients, and TNBC-related cell lines were cultured. mRNA expression was determined using reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR). Functional parameters were assessed through the following experimental methods: the cell counting kit-8 (CCK-8) assay was employed to evaluate proliferation capacity, the Transwell was conducted to assess migration and invasion, and the dual-luciferase assay was performed to confirm the targeted binding relationships.

Results

GAPLINC was significantly upregulated in TNBC tissues and cell lines (P < 0.001), and its expression was closely correlated with poor clinical prognosis. Similarly, miR-331-3p was markedly downregulated in TNBC samples (P < 0.001), while IGF2BP1 expression was significantly overexpressed (P < 0.001). Silencing GAPLINC effectively suppressed proliferation, migration, and invasion, accompanied by a notable upregulation miR-331-3p expression (P < 0.001). Importantly, inhibition of miR-331-3p partially reversed the suppressive effects induced by GAPLINC knockdown. Furthermore, miR-331-3p targeted IGF2BP1. Additional knockdown of IGF2BP1 counteracted this reversal effect, thereby effectively abrogating the tumor-promoting function of GAPLINC.

Conclusion

This study identified GAPLINC as a crucial oncogenic lncRNA in TNBC. It promoted tumor progression by competitively binding to miR-331-3p, thereby derepressing its target IGF2BP1. These findings not only elucidated a new GAPLINC/miR-331-3p/IGF2BP1 regulatory axis, but also highlighted that GAPLINC may be a potential prognostic biomarker for triple-negative breast cancer.