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

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.

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Journal
World Journal of Surgical Oncology
Published
2026-05-18
DOI
https://doi.org/10.1186/s12957-026-04387-3
Primary Topic
Cancer-related molecular mechanisms research
Type
article
Field-Weighted Citation Impact
0.00

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article

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

S L Zhang, Guijun Yan, Ziguo Yang, Shaocong Yan et al.
World Journal of Surgical Oncology
Cancer-related molecular mechanisms research
article

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

S L Zhang, Guijun Yan, Ziguo Yang, Shaocong Yan, Lina Huang, Wenyan Wang
article en

Abstract

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.

World Journal of Surgical Oncology
Xuzhou Medical College (CN), Beijing Tian Tan Hospital (CN), Jingdezhen University (CN), Affiliated Hospital of Youjiang Medical University for Nationalities (CN), Baise University (CN), Xuzhou No.1 People's Hospital (CN)
Wu Jieping Medical Foundation
No poverty
Openalex Percentile: Top 7%
Cancer-related molecular mechanisms research
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