Evidence map›Paper›PMID 33125151›Full record

Observational studyOncology reports2020

lncRNA KTN1‑AS1 promotes glioma cell proliferation and invasion by negatively regulating miR‑505‑3p.

Yulong Mu, Qiang Tang, Haiyan Feng, Luwen Zhu, Yan Wang

Open access · hybridAbstract readObservational Study
In one paragraph

Observational study in Oncology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 27 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Yulong Mu *Department of Surgery, Hanan Branch of The Second Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang 150001, P.R. China.
Qiang Tang *Rehabilitation Medicine Center of the Second Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang 150001, P.R. China.
Haiyan FengShanghai Public Health Clinical Center, Jinshan, Shanghai 200001, P.R. China.
Luwen ZhuRehabilitation Medicine Center of the Second Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang 150001, P.R. China.
Yan WangRehabilitation Medicine Center of the Second Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang 150001, P.R. China.
Heilongjiang University of Chinese Medicine · CNShanghai Public Health Clinical Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma (GBM) is one of the most prevalent and aggressive central nervous tumors with high mobility and mortality. The prognosis of patients with GBM is poor. It is therefore essential to explore the therapeutic strategies for the treatment of GBM. Previous studies have demonstrated that the long non‑coding RNA (lncRNA) Kinectin 1‑Antisense RNA 1 (KTN1‑AS1) can participate in the development of several types of cancer. However, the underlying mechanism of KTN1‑AS1 in GBM remains unknown. The present study aimed to determine the potential role of KTN1‑AS1 in GBM. In this study, reverse transcription quantitative PCR analysis was conducted and the results demonstrated that KTN1‑AS1 was upregulated in GBM tissues and cell lines compared with normal tissues and astrocytes (NHA). Furthermore, KTN1‑AS1 knockdown decreased the viability and invasive ability of glioma cells in vitro and in vivo. In addition, high level of KTN1‑AS1 was correlated with poor prognosis in TCGA GBM database. Furthermore, microRNA‑505‑3p (miR‑505‑3p) was a promising target of KTN1‑AS1, and the suppressing effects of miR‑505‑3p on cell proliferation and invasive ability was reversed by downregulating KTN1‑AS1. Taken together, the results from the present provided novel insights into the roles of KTN1‑AS1 in GBM, and suggested that the KTN1‑AS1/miR‑505‑3p axis may be considered as a novel therapeutic target for the treatment of patients with GBM.

Indexed as

AdultAgedAnimalsAstrocytesBrainBrain NeoplasmsCell Line, TumorCell MovementCell ProliferationCell SurvivalDatasets as TopicDown-RegulationFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesGlioblastomaMicroRNAsMIRN505 microRNA, humanRNA, Long NoncodinggliomainvasionKTN1-AS1long non-coding RNAmiR-505-3p

Identifiers

PMID33125151
PMCPMC7640367
OpenAlexW3093921845

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.