ArticleBioscience reports2019
LncRNA LUCAT1 facilitates tumorigenesis and metastasis of triple-negative breast cancer through modulating miR-5702.
Article in Bioscience reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.
- Prognostic value of long non-coding RNAs in triple negative breast cancer: A PRISMA-compliant meta-analysis.Medicine · 2020Pooled it
- LUCAT1 promotes stemness in head and neck squamous cell carcinoma by sponging miR-128.Frontiers in oncology · 2026Article
- Hypoxia-induced exosomal LUCAT1 promotes osimertinib resistance in lung adenocarcinoma by stabilizing c-MET.Cell death & disease · 2025Article
- LncRNA LUCAT1 as a prognostic biomarker in cholangiocarcinoma through targeting miR-141-3p: clinical and functional insights.Hereditas · 2025Article
- Molecular Mechanism of lncRNAs in Regulation of Breast Cancer Metastasis; a Comprehensive Review.Cell biochemistry and biophysics · 2025Review
- LUCAT1-Mediated Competing Endogenous RNA (ceRNA) Network in Triple-Negative Breast Cancer.Cells · 2024Article
- The lncRNA AFAP1-AS1 is upregulated in metastatic triple-negative breast tumors and controls hypoxia-activated vasculogenic mimicry and angiogenesis.BMC cancer · 2024Article
- Long non‑coding RNA lung cancer‑associated transcript 1 regulates ferroptosis via microRNA‑34a‑5p‑mediated GTP cyclohydrolase 1 downregulation in lung cancer cells.International journal of oncology · 2024Article
- Article
- The Role of Long Noncoding RNAs (lncRNAs) in Esophageal Cancer Therapy Resistance and Metastasis.Biomedicines · 2024Review
- Mechanisms of tamoxifen resistance: insight from long non-coding RNAs.Frontiers in oncology · 2024Review
- Long-chain noncoding RNA LINC01569 upregulates filamin A-interacting protein 1-like to prevent metastasis of triple-negative breast cancer via sponging miR-300.Cancer biomarkers : section A of Disease markers · 2024Article
- Targeted therapy approaches for epithelial-mesenchymal transition in triple negative breast cancer.Frontiers in oncology · 2024Review
- Deciphering the code: the pivotal role of lncRNAs in advancing TNBC therapy.Frontiers in oncology · 2024Review
- Roles of lncRNA in the diagnosis and prognosis of triple-negative breast cancer.Journal of Zhejiang University. Science. B · 2023Review
- Exploiting Long Non-Coding RNAs and Circular RNAs as Pharmacological Targets in Triple-Negative Breast Cancer Treatment.Cancers · 2023Review
- Metformin and long non-coding RNAs in breast cancer.Journal of translational medicine · 2023Review
- Review
- PBX3-activated DLG1-AS1 can promote the proliferation, invasion, and migration of TNBC cells by sponging miR-16-5p.Molecular therapy oncolytics · 2022Article
- SNHG1-miR-186-5p-YY1 feedback loop alleviates hepatic ischemia/reperfusion injury.Cell cycle (Georgetown, Tex.) · 2022Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer (TNBC) is a subtype of aggressive breast cancer with high recurrence and poor survival. Emerging evidence has indicated that long non-coding RNAs (lncRNAs) play pivotal roles in the development and progression of multiple cancers. Although there are substantial studies revealing that lung cancer-associated transcript 1 (LUCAT1) functions as a tumor promotor in various human cancers, the molecular mechanism of LUCAT1 in TNBC remains largely to be explored. In our study, we identified that LUCAT1 expression was dramatically enhanced in TNBC samples and cells. High LUCAT1 expression was strongly associated with advanced stages and poor prognosis of TNBC. LUCAT1 contributed to TNBC development through accelerating cell proliferation, cell cycle progression and metastasis as well as attenuating cell apoptosis. Moreover, miR-5702 was proved to directly bind to LUCAT1 and be negatively modulated by LUCAT1. Knockdown of miR-5702 reversed the suppressing influences of LUCAT1 depletion on TNBC progression. In conclusion, it was the first investigation to shed light on the significant function and underlying regulatory mechanism of LUCAT1 in TNBC tumorigenesis. We validated that LUCAT1 induced tumorigenesis and metastasis of TNBC via miR-5702, which provided clues for improving the treatment of TNBC.
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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.