LINC01128 Affects Triple-Negative Breast Cancer Progression Through Targeting miR-32-5p.

Area of Science:

• Oncology
• Molecular Biology
• Genetics

Background:

• Triple-negative breast cancer (TNBC) is an aggressive subtype with limited therapeutic options.
• Long non-coding RNAs (lncRNAs) play crucial roles in cancer development and progression.
• Understanding the molecular mechanisms underlying TNBC is essential for developing novel treatments.

Purpose of the Study:

• To investigate the expression and clinical significance of LINC01128 in TNBC.
• To determine if LINC01128 regulates TNBC cell behaviors by targeting miR-32-5p through the competing endogenous RNA (ceRNA) mechanism.
• To explore LINC01128 as a potential therapeutic target for TNBC.

Main Methods:

• Quantitative real-time PCR (qPCR) to measure LINC01128 and miR-32-5p expression in TNBC tissues and cell lines.
• Dual-luciferase reporter assay to confirm the direct binding between LINC01128 and miR-32-5p.
• Cell proliferation, apoptosis, and migration assays (CCK-8, flow cytometry, Transwell) to assess the functional impact of LINC01128.
• Bioinformatic analyses (miRDB, miRWalk) for target gene prediction and pathway enrichment.

Main Results:

• LINC01128 was significantly upregulated in TNBC tissues and cells compared to normal controls.
• High LINC01128 expression correlated with advanced TNBC and served as an independent risk factor.
• miR-32-5p was downregulated in TNBC and showed a negative correlation with LINC01128.
• LINC01128 promoted TNBC cell proliferation and migration while inhibiting apoptosis by sponging miR-32-5p.
• Target genes of miR-32-5p were enriched in cancer-related pathways.

Conclusions:

• LINC01128 is highly expressed in TNBC and drives tumor progression.
• The LINC01128/miR-32-5p ceRNA axis plays a critical role in regulating TNBC cell behaviors.
• LINC01128 represents a promising molecular marker and therapeutic target for TNBC.