Breast cancer (Dove Medical Press) · 2026
miR-1911-3p Regulates Malignant Biological Behaviors and Glycolytic Activity of Triple-Negative Breast Cancer via FBLN5.
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Kong Linna, Zhang Huihui, Sui Xufang, Peng Xueping, Sun Tiantian
Аннотация
BACKGROUND AND OBJECTIVES: Based on previous reports demonstrating the clinical potential of miR-1911-3p in breast cancer, its function and mechanisms in the development of TNBC were investigated, aiming to identify a novel biomarker.
MATERIALS AND METHODS: Paired tissues were sampled from 128 TNBC patients, and miR-1911-3p levels were compared between tumor and normal tissues. The clinical significance of miR-1911-3p was evaluated from the perspective of disease severity and patients' prognosis. In vitro, the regulatory effects of miR-1911-3p on the malignant biological behaviors were assessed based on cell growth, motility, and glycolytic activity in MDA-MB-231 and HCC1806 cells. The mechanism evaluation was performed focusing on FBLN5 through luciferase reporter assay and related reversal experiments by co-regulating miR-1911-3p and FBLN5.
RESULTS: Significant upregulation of miR-1911-3p was observed in tumor tissues of TNBC patients (fold change of 1.35), which was associated with advanced TNM stage, higher Ki67 levels, and occurrence of lymph node metastasis. miR-1911-3p (HR = 3.036) was identified as an independent prognostic factor predicting 5-year recurrence-free survival (log‑rank P = 0.036) of TNBC patients. Consistent elevation of miR-1911-3p was also observed in TNBC cells, and its knockdown dramatically suppressed cell proliferation, migration, and invasion. Glycolytic activity was revealed to mediate the regulation of cell biological functions. FBLN5 was identified as a downstream target of miR-1911-3p, and negative regulation of its expression by miR-1911-3p was observed. Silencing FBLN5 could reverse the tumor‑suppressive effect of miR-1911-3p on TNBC cells, which was considered the major molecular mechanism.
CONCLUSION: miR-1911-3p was identified as an independent prognostic biomarker for TNBC. Different from previously reporter miRNAs, miR-1911-3p regulated glycolytic activity-dependent cell growth and motility by targeting FBLN5, indicating its potential in serving as therapeutic target for TNBC.
MATERIALS AND METHODS: Paired tissues were sampled from 128 TNBC patients, and miR-1911-3p levels were compared between tumor and normal tissues. The clinical significance of miR-1911-3p was evaluated from the perspective of disease severity and patients' prognosis. In vitro, the regulatory effects of miR-1911-3p on the malignant biological behaviors were assessed based on cell growth, motility, and glycolytic activity in MDA-MB-231 and HCC1806 cells. The mechanism evaluation was performed focusing on FBLN5 through luciferase reporter assay and related reversal experiments by co-regulating miR-1911-3p and FBLN5.
RESULTS: Significant upregulation of miR-1911-3p was observed in tumor tissues of TNBC patients (fold change of 1.35), which was associated with advanced TNM stage, higher Ki67 levels, and occurrence of lymph node metastasis. miR-1911-3p (HR = 3.036) was identified as an independent prognostic factor predicting 5-year recurrence-free survival (log‑rank P = 0.036) of TNBC patients. Consistent elevation of miR-1911-3p was also observed in TNBC cells, and its knockdown dramatically suppressed cell proliferation, migration, and invasion. Glycolytic activity was revealed to mediate the regulation of cell biological functions. FBLN5 was identified as a downstream target of miR-1911-3p, and negative regulation of its expression by miR-1911-3p was observed. Silencing FBLN5 could reverse the tumor‑suppressive effect of miR-1911-3p on TNBC cells, which was considered the major molecular mechanism.
CONCLUSION: miR-1911-3p was identified as an independent prognostic biomarker for TNBC. Different from previously reporter miRNAs, miR-1911-3p regulated glycolytic activity-dependent cell growth and motility by targeting FBLN5, indicating its potential in serving as therapeutic target for TNBC.