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Updated: Sep 13, 2025

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
LINC01232 regulates miR-516a-5p/BCL9 axis to promote triple-negative breast cancer progression
Wei Liu1, Yunfeng Niu2, Jie An3
1Department of General Surgery, Bethune International Peace Hospital, No. 398 Zhongshan West Road, Qiaoxi District, Shijiazhuang, Hebei, China. liuweihpyy2023@163.com.
Abstract:
Triple-negative breast cancer (TNBC) is characterised by an absence of the oestrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2), for which there are few therapeutic options and the prognosis is poor. This research sought to explore the particular function of the long non-coding RNA (lncRNA) LINC01232 in TNBC and its regulatory impacts on the miR-516a-5p/BCL9 pathway. In this study, quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to determine the expression level of LINC01232 in TNBC tissues. We also examined its regulatory influences on miR-516a-5p and BCL9 via cellular function tests and a luciferase reporter experiment. Evaluated the effect of LINC01232 silencing on proliferation, migration and invasion of breast cancer cells. Results showed that LINC01232 expression was abnormally high in TNBC tissues in comparison to normal tissues. Inhibition of LINC01232 expression markedly impeded breast cancer cell proliferation, clone formation, migration and invasion. We found that LINC01232 competes with miR-516a-5p for binding, thereby reducing its expression and subsequently increasing BCL9 expression. In conclusion, our results indicate that LINC01232 facilitates the malignant development of TNBC through the miR-516a-5p/BCL9 pathway, providing fresh perspectives on the pathogenesis of TNBC and pinpointing potential therapeutic targets.
Insights
Triple-negative breast cancer (TNBC) involves high LINC01232 levels. Inhibiting this long non-coding RNA (lncRNA) reduces TNBC cell growth and spread by affecting the miR-516a-5p/BCL9 pathway.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Triple-negative breast cancer (TNBC) lacks targeted therapies and has a poor prognosis.
- The role of long non-coding RNAs (lncRNAs) in TNBC pathogenesis is an area of active investigation.
- Identifying novel molecular pathways is crucial for developing effective TNBC treatments.
Purpose of the Study:
- To investigate the function of the lncRNA LINC01232 in TNBC.
- To elucidate the regulatory mechanism of LINC01232 involving the miR-516a-5p/BCL9 pathway.
- To assess LINC01232 as a potential therapeutic target for TNBC.
Main Methods:
- Quantitative reverse transcription polymerase chain reaction (qRT-PCR) to measure LINC01232 expression in TNBC tissues.
- Luciferase reporter assays and cellular function tests to analyze the interaction between LINC01232, miR-516a-5p, and BCL9.
- In vitro experiments evaluating the impact of LINC01232 silencing on TNBC cell proliferation, migration, and invasion.
Main Results:
- LINC01232 expression was significantly upregulated in TNBC tissues compared to normal tissues.
- Silencing LINC01232 inhibited proliferation, colony formation, migration, and invasion of breast cancer cells.
- LINC01232 acts as a competing endogenous RNA (ceRNA) for miR-516a-5p, leading to increased BCL9 expression.
Conclusions:
- LINC01232 promotes TNBC malignant progression via the miR-516a-5p/BCL9 pathway.
- LINC01232 represents a potential diagnostic biomarker and therapeutic target for TNBC.
- This study offers new insights into the molecular mechanisms underlying TNBC development.
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