Evidence map›Paper›PMID 33469379›Full record

ArticleCancer management and research2021

Long Non-Coding RNA UBA6-AS1 Promotes the Malignant Properties of Glioblastoma by Competitively Binding to microRNA-760 and Enhancing Homeobox A2 Expression.

Feifei Cheng, Jiang Liu, Yundong Zhang, Qiuxiang You, Bo Chen, Jing Cheng, Chunyan Deng

RetractedAbstract readRetracted Publication
In one paragraph

Article in Cancer management and research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
  2. Review
  3. Frontiers in molecular biosciences · 2022
    Article
  4. Article
  5. Article
  6. Non-Coding RNAs and Brain Tumors: Insights Into Their Roles in Apoptosis.Frontiers in cell and developmental biology · 2021
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Feifei ChengDepartment of Neurology, The Third Affiliated Hospital of Chongqing Medical University, Chongqing 401120, People's Republic of China.
Jiang LiuDepartment of Neurology, The Third Affiliated Hospital of Chongqing Medical University, Chongqing 401120, People's Republic of China.
Yundong ZhangDepartment of Neurology, The Third Affiliated Hospital of Chongqing Medical University, Chongqing 401120, People's Republic of China.
Qiuxiang YouDepartment of Neurology, The Third Affiliated Hospital of Chongqing Medical University, Chongqing 401120, People's Republic of China.
Bo ChenDepartment of Pharmacology, College of Pharmacy, Chongqing Medical University, Chongqing 401120, People's Republic of China.
Jing ChengDepartment of Neurology, The Third Affiliated Hospital of Chongqing Medical University, Chongqing 401120, People's Republic of China.
Chunyan DengDepartment of Neurology, The Third Affiliated Hospital of Chongqing Medical University, Chongqing 401120, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe dysregulation of long non-coding RNAs is a frequent finding in glioblastoma (GBM) and is considered as a crucial mechanism contributing to GBM oncogenesis and progression. The biological roles and underlying mechanisms of action of UBA6 antisense RNA 1 (UBA6-AS1) in GBM have been rarely investigated. Therefore, the aim of the present study was to investigate in detail the role of UBA6-AS1 in the modulation of the malignant properties of GBM and explore the possible underlying mechanism(s).

methodsThe expression of UBA6-AS1 in GBM was determined via reverse transcription-quantitative PCR. Cell Counting Kit-8 assay, flow cytometric analysis, Transwell migration and invasion assays, and in vivo tumorigenicity assay were applied to elucidate the biological effects of UBA6-AS1 on GBM cells. The possible biological events associated with UBA6-AS1 were investigated by luciferase reporter, RNA immunoprecipitation (RIP) and rescue assays.

resultsUBA6-AS1 was overexpressed in GBM, which was consistent with the data from The Cancer Genome Atlas database. In the case of UBA6-AS1 depletion, GBM cell proliferation, migration and invasion were notably decreased and cell apoptosis was enhanced in vitro. Additionally, knockdown of UBA6-AS1 suppressed the proliferation of GBM cells in vivo. Mechanistically, UBA6-AS1 functioned as a competing endogenous RNA by adsorbing miR-760 and, consequently, upregulating homeobox A2 (HOXA2) expression. Rescue experiments demonstrated that the UBA6-AS1 silencing-mediated regulatory effects on GBM cells were reversed by the decrease of miR-760 or restoration of HOXA2 expression.

conclusionTherefore, the results of the present study revealed that UBA6-AS1 promoted the malignant progression of GBM via targeting the miR-760/HOXA2 axis, thereby representing a promising effective target for the treatment of GBM.

Indexed as

glioblastomahomeobox A2long non-coding RNAUBA6 antisense RNA 1

Identifiers

PMID33469379
PMCPMC7813458

What Socratic 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 Socratic graph.