ArticleOncoTargets and therapy2019
Long Non-Coding RNA BCAR4 Promotes Growth, Invasion and Tumorigenicity by Targeting miR-2276 to Upregulate MMP7 Expression in Glioma.
Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Long non-coding RNAs in glioblastoma: from molecular drivers to therapeutic targets.Frontiers in immunology · 2026Review
- Long Non-Coding RNAs in Malignant Human Brain Tumors: Driving Forces Behind Progression and Therapy.International journal of molecular sciences · 2025Review
- Shedding light on function of long non-coding RNAs (lncRNAs) in glioblastoma.Non-coding RNA research · 2024Review
- Article
- E2F transcription factor 1/small nucleolar RNA host gene 18/microRNA-338-5p/forkhead box D1: an important regulatory axis in glioma progression.Bioengineered · 2022Article
- The role of long non-coding RNA BCAR4 in human cancers.Human cell · 2021Review
- COL5A1 Serves as a Biomarker of Tumor Progression and Poor Prognosis and May Be a Potential Therapeutic Target in Gliomas.Frontiers in oncology · 2021Article
- Exosomal miR-2276-5p in Plasma Is a Potential Diagnostic and Prognostic Biomarker in Glioma.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveLong non-coding RNA breast cancer anti-estrogen resistance 4 (BCAR4) has been recognized as a proto-oncogene in various malignancies. It has been reported to be highly expressed and promote cell proliferation in glioma. However, its additional roles in gliomagenesis remain largely unclear. This research intends to investigate the impact and internal molecular mechanism of BCAR4 on glioma cell growth, invasion and tumorigenesis.
methodsBCAR4 expression was examined by qPCR in 30 cases of graded glioma specimens and 7 glioblastoma (GBM) cell lines compared with respective controls. Its potential prognostic value was evaluated by Kaplan-Meier survival analysis. The biological roles of BCAR4 in gliomagenesis were verified by CCK-8, transwell and intracranial xenograft assays successively. qPCR and RNA pull-down assays were applied to study the relationship between BCAR4 and miR-2276. Then, qPCR, Western blot and luciferase reporter assays were used to validate the targeting of matrix metallopeptidase 7 (MMP7) by miR-2276 and the regulation of MMP7 by BCAR4. Finally, MMP7 was restored in BCAR4-silenced GBM cells and the rescue effects were determined by CCK-8 and transwell assays.
resultsBCAR4 expression was increased in glioma tissues and GBM cell lines, and its high expression positively correlated with advanced grades and worse prognosis. Functional assays verified that knockdown of BCAR4-inhibited cell growth and invasion in vitro, and impaired tumor formation in vivo. Mechanistically, we found that BCAR4 could act as a competing endogenous RNA (ceRNA) by targeting miR-2276 to upregulate MMP7 expression. Importantly, MMP7 restoration effectively rescued the inhibitory modulations on GBM cell growth and invasion caused by BCAR4 knockdown.
conclusionOur findings identified the essential roles of the BCAR4/miR-2276/MMP7 axis in gliomagenesis and provided novel insights on glioma therapy.
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