LINC01537 Regulates Malignant Phenotypes and Predicts Prognosis in Breast Cancer, and Its Bioinformatics Analysis

Breast cancer is a highly heterogeneous malignancy and constitutes one of the leading health threats to women globally. This study aimed to investigate the expression profile, clinical relevance, and molecular mechanisms of LINC01537 in breast cancer. Quantitative real-time PCR (qRT-PCR) was performed to detect the expression of LINC01537, miR-138-5p, and EZH2 in breast cancer tissues and cells. The Kaplan-Meier method was used for survival analysis, and forest plots were constructed to evaluate the prognostic significance of LINC01537. To explore the role of LINC01537 in BT549 and SK-BR-3 cells proliferation, apoptosis, migration, and invasion, LINC01537 was knocked down in BT549 and SK-BR-3 cells, followed by CCK-8, flow cytometry, and Transwell assays. A potential competing endogenous RNA (ceRNA) regulatory network was investigated through bioinformatics analysis, dual-luciferase reporter assays, and correlation analyses. Rescue experiments were further performed to confirm that LINC01537 modulates breast cancer progression via the miR-138-5p/EZH2 axis. LINC01537 was significantly upregulated in breast cancer tissues and cell lines compared to normal controls. High LINC01537 expression was associated with poor survival outcomes in patients. Knockdown of LINC01537 markedly suppressed proliferation, migration, and invasion, while promoting apoptosis in BT549 and SK-BR-3 cells. Mechanically, LINC01537 functioned as a ceRNA by sponging miR-138-5p, thereby abrogating its inhibitory effect on the target gene EZH2. Rescue experiments suggested that the inhibition of the malignant phenotypes of BT549 and SK-BR-3 cells caused by LINC01537 knockdown was rescued by miR-138-5p inhibition. The LINC01537/miR-138-5p/EZH2 ceRNA axis is involved in the progression of TNBC and HER2-positive breast cancer subtypes. In vitro data indicates that LINC01537 is a potential therapeutic candidate for TNBC and HER2-positive breast cancer, while further in vivo animal validation is required to support its translational application.

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Journal
Journal of Biochemical and Molecular Toxicology
Published
2026-10-18
DOI
https://doi.org/10.1002/jbt.71123
Primary Topic
Cancer-related molecular mechanisms research
Type
article
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article

LINC01537 Regulates Malignant Phenotypes and Predicts Prognosis in Breast Cancer, and Its Bioinformatics Analysis

Libo Shi, Y. P. Guo
Journal of Biochemical and Molecular Toxicology
Cancer-related molecular mechanisms research
article

LINC01537 Regulates Malignant Phenotypes and Predicts Prognosis in Breast Cancer, and Its Bioinformatics Analysis

Libo Shi, Y. P. Guo
article en

Abstract

Breast cancer is a highly heterogeneous malignancy and constitutes one of the leading health threats to women globally. This study aimed to investigate the expression profile, clinical relevance, and molecular mechanisms of LINC01537 in breast cancer. Quantitative real-time PCR (qRT-PCR) was performed to detect the expression of LINC01537, miR-138-5p, and EZH2 in breast cancer tissues and cells. The Kaplan-Meier method was used for survival analysis, and forest plots were constructed to evaluate the prognostic significance of LINC01537. To explore the role of LINC01537 in BT549 and SK-BR-3 cells proliferation, apoptosis, migration, and invasion, LINC01537 was knocked down in BT549 and SK-BR-3 cells, followed by CCK-8, flow cytometry, and Transwell assays. A potential competing endogenous RNA (ceRNA) regulatory network was investigated through bioinformatics analysis, dual-luciferase reporter assays, and correlation analyses. Rescue experiments were further performed to confirm that LINC01537 modulates breast cancer progression via the miR-138-5p/EZH2 axis. LINC01537 was significantly upregulated in breast cancer tissues and cell lines compared to normal controls. High LINC01537 expression was associated with poor survival outcomes in patients. Knockdown of LINC01537 markedly suppressed proliferation, migration, and invasion, while promoting apoptosis in BT549 and SK-BR-3 cells. Mechanically, LINC01537 functioned as a ceRNA by sponging miR-138-5p, thereby abrogating its inhibitory effect on the target gene EZH2. Rescue experiments suggested that the inhibition of the malignant phenotypes of BT549 and SK-BR-3 cells caused by LINC01537 knockdown was rescued by miR-138-5p inhibition. The LINC01537/miR-138-5p/EZH2 ceRNA axis is involved in the progression of TNBC and HER2-positive breast cancer subtypes. In vitro data indicates that LINC01537 is a potential therapeutic candidate for TNBC and HER2-positive breast cancer, while further in vivo animal validation is required to support its translational application.

Journal of Biochemical and Molecular ToxicologyVol. 40(11)
Chengde Medical University (CN), People's Hospital of Cangzhou (CN)
Openalex Percentile: Top 18%
Cancer-related molecular mechanisms research
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