Evidence map›Paper›PMID 42893420›Full record

ArticleJournal of biochemical and molecular toxicology2026

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

Yuetong Guo, Libo Shi

Abstract read
In one paragraph

Article in Journal of biochemical and molecular toxicology, 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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0citing papers in PubMed
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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Yuetong GuoChengde Medical University, Chengde, Hebei, China.
Libo ShiDepartment of Breast Surgery, Cangzhou People's Hospital, Cangzhou, Hebei, China.ORCID https://orcid.org/0009-0004-7272-0178

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Breast NeoplasmsComputational BiologyGene Expression Regulation, NeoplasticRNA, Long NoncodingRNA, NeoplasmApoptosisCell Line, TumorCell MovementCell ProliferationEnhancer of Zeste Homolog 2 ProteinFemaleHumansMicroRNAsPhenotypePrognosisRNA, Competitive EndogenousEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanMicroRNAsMIRN138 microRNA, humanRNA, Competitive EndogenousRNA, Long NoncodingRNA, Neoplasmbreast cancerEZH2LINC01537miR‐138‐5pprognosis

Identifiers

PMID42893420
PMCPMC13676844

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.