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Abstract Objectives This study explored the functional role of LINC01943 in triple-negative breast cancer (TNBC) development and prognosis to improve patient survival outcomes. Methods This study included 111 TNBC patients. LINC01943 and miR-224-5p expression levels in tumor tissues and TNBC cell lines (BT-549, MDA-MB-231, SUM-159, HCC1806) were analyzed by real-time quantitative PCR. Cox regression analyses and Kaplan-Meier survival curves confirmed the association between LINC01943 and TNBC prognosis. Luciferase assays validated the interaction between LINC01943 and miR-224-5p, while functional assays assessed their impact on proliferation, invasion, and apoptosis of TNBC cells. Bioinformatics analysis combined with luciferase assays preliminarily validated PLOD2 as a direct target of miR-224-5p. Western blot was used to detect protein expression levels. Results Compared with adjacent normal tissues and MCF-10, LINC01943 is upregulated in TNBC tissues and cell lines, while miR-224-5p is downregulated, and the two are negatively correlated in TNBC tumor tissues. Elevated LINC01943 expression correlated with advanced tumor node metastasis (TNM) stage, lymph node metastasis (LNM), and poorer 5-year survival in TNBC patients. LINC01943, TNM stage, and LNM were identified as prognostic predictors for TNBC. LINC01943 promoted tumor growth by enhancing cell proliferation and invasion while suppressing apoptosis through miR-224-5p regulation. PLOD2 was identified as the direct functional target of miR-224-5p, serving as the key downstream mediator of the LINC01943/miR-224-5p axis in regulating EMT and FAK signaling in TNBC. Conclusions LINC01943 is a novel prognostic biomarker for TNBC. The LINC01943/miR-224-5p/PLOD2 axis promotes tumor progression by activating FAK signaling and EMT, offering a promising therapeutic target.