World journal of surgical oncology · 2026
Lnc RNA GAPLINC affects triple-negative breast cancer progression through the miR-331-3p/IGF2BP1 axis.
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Wang Wenya, Huang Lina, Zhan Siyue, Yan Ziguo, Yan Shaocong, Yan Guijun
Аннотация
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.
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.