Evidence map›Paper›PMID 32547064›Full record

ArticleOncoTargets and therapy2020

SP1-Mediated Upregulation of lncRNA LINC01614 Functions a ceRNA for miR-383 to Facilitate Glioma Progression Through Regulation of ADAM12.

Hao Wang, Jiang Wu, Wei Guo

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.8field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Unraveling the role of specificity protein 1 in gliomas: pathophysiology and clinical implications.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  2. LINC01614: A Potential Therapeutic Target in Astrocytoma Progression.Journal of cellular and molecular medicine · 2025
    Article
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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

3 authors at 2 institutions in 1 country.

Hao WangDepartment of Neurosurgery, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, Shenzhen, Guangdong, People's Republic of China.
Jiang WuDepartment of Neurosurgery, Hebei General Hospital, Shijiazhuang, Hebei, People's Republic of China.
Wei GuoDepartment of Neurosurgery, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, Shenzhen, Guangdong, People's Republic of China.
Jinan University · CNHebei General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLong non-coding RNAs (lncRNAs) play an imperative role in tumorigenesis, but few lncRNAs have been functionally characterized in glioma. The aim of the present study was to identify the role of long non-coding RNA LINC01614 (LINC01614) in glioma development and explore the underlying mechanisms of LINC01614/miR-383/ADAM12 axis. PATIENTS AND

methodsLncRNA expression in glioma specimens was measured by lncRNA microarray and qRT-PCR. The prognostic value of LINC01614 expression was statistically analyzed in 112 glioma patients. Loss-of-function experiments were conducted to investigate the biological functions of LINC01614 in vitro. Luciferase analyses, ChIP assays, and RNA pull-down were performed to determine the underlying LINC01614 mechanisms.

resultsWe identified a novel glioma-related lncRNA LINC01614 by analyzing TCGA datasets. The distinct upregulation of LINC01614 was observed in both glioma specimens and cell lines using RT-PCR. We also observed that LINC01614 upregulation was induced by nuclear transcription factor SP1. Clinical assays revealed that high levels of LINC01614 were associated with KPS, WHO grade and shorter overall survival of glioma patients. Multivariate analysis further confirmed that LINC01614 was an independent prognostic marker for glioma patients. Besides, functional assays displayed that silence of LINC01614 knockdown distinctly inhibited cell growth, migration and invasion and promoted cell apoptosis in glioma cells. LINC01614 expression was enriched in the cytoplasm of glioma cells. Mechanistic investigation revealed that LINC01614 functioned as a competing endogenous RNA to upregulate a disintegrin and metalloproteinase 12 (ADAM12) by sponging miR-383.

conclusionOverall, these findings showed that SP1-induced upregulation of LINC01614 promoted glioma malignant progression via modulating the miR-383/ADAM12 axis, which may provide a promising therapy for glioma.

Indexed as

ADAM12gliomalncRNA LINC01614metastasismiR-383prognosis

Identifiers

PMID32547064
PMCPMC7244248
OpenAlexW3024148459

What OpenQuestion holds

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Registered trials

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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.