ArticleBreast cancer (Dove Medical Press)2026
LINC01128 Affects Triple-Negative Breast Cancer Progression Through Targeting miR-32-5p.
Article in Breast cancer (Dove Medical Press), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: To clarify the expression and clinical significance of LINC01128 in triple-negative breast cancer (TNBC), investigate whether it regulates the biological behaviors of TNBC cells by targeting miR-32-5p via the ceRNA mechanism, and explore new therapeutic targets. Methods: Tumor tissues and corresponding adjacent normal tissues from 76 TNBC patients were collected, and the patients' clinicopathological data were gathered. Experiments were conducted using the human normal breast epithelial cell line MCF-12F and multiple TNBC cell lines. Quantitative real-time PCR (qPCR) was used to detect the relative expressions of LINC01128 and miR-32-5p; dual-luciferase reporter assay was performed to verify the targeted binding relationship between the two. CCK-8 assay, flow cytometry, and Transwell assay were used to detect cell proliferation, apoptosis, and migration abilities, respectively. Target gene prediction and GO/KEGG enrichment analyses were carried out by combining databases such as miRDB and miRWalk. Results: LINC01128 was highly expressed in TNBC tissues and cells (P<0.01), and its high expression was an independent risk factor for advanced TNBC (OR=6.635, P=0.001). miR-32-5p was lowly expressed in TNBC (P<0.01) and showed a significant negative correlation with LINC01128 (r=-0.699, P<0.001), with a direct targeted binding between the two. LINC01128 promoted TNBC cell proliferation and migration and inhibited apoptosis by suppressing miR-32-5p (all P<0.01). The target genes of miR-32-5p were enriched in tumor-related pathways. Conclusion: LINC01128 is highly expressed in TNBC and promotes tumor progression by targeting and suppressing miR-32-5p via the ceRNA mechanism, which can serve as a potential molecular marker and therapeutic target for TNBC.
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