Evidence map›Paper›PMID 31059060›Full record

ArticleMolecular medicine reports2019

Long non‑coding RNA NORAD promotes cell proliferation and glycolysis in non‑small cell lung cancer by acting as a sponge for miR‑136‑5p.

Wei Gao, Ting Weng, Lifang Wang, Bin Shi, Wenshu Meng, Xiaoyu Wang, Ying Wu, Liang Jin, Lijuan Fei

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 40 citations in OpenAlex.

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  15. Competing endogenous RNAs in lung cancer.Cancer biology & medicine · 2021
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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

9 authors at 1 institution in 1 country.

Wei GaoDepartment of Respiratory Medicine, Suqian People's Hospital of Nanjing Drum Tower Hospital Group, Suqian, Jiangsu 223800, P.R. China.
Ting WengDepartment of Respiratory Medicine, Suqian People's Hospital of Nanjing Drum Tower Hospital Group, Suqian, Jiangsu 223800, P.R. China.
Lifang WangDepartment of Respiratory Medicine, Suqian People's Hospital of Nanjing Drum Tower Hospital Group, Suqian, Jiangsu 223800, P.R. China.
Bin ShiDepartment of Respiratory Medicine, Suqian People's Hospital of Nanjing Drum Tower Hospital Group, Suqian, Jiangsu 223800, P.R. China.
Wenshu MengDepartment of Respiratory Medicine, Suqian People's Hospital of Nanjing Drum Tower Hospital Group, Suqian, Jiangsu 223800, P.R. China.
Xiaoyu WangDepartment of Respiratory Medicine, Suqian People's Hospital of Nanjing Drum Tower Hospital Group, Suqian, Jiangsu 223800, P.R. China.
Ying WuDepartment of Respiratory Medicine, Suqian People's Hospital of Nanjing Drum Tower Hospital Group, Suqian, Jiangsu 223800, P.R. China.
Liang JinDepartment of Respiratory Medicine, Suqian People's Hospital of Nanjing Drum Tower Hospital Group, Suqian, Jiangsu 223800, P.R. China.
Lijuan FeiDepartment of Respiratory Medicine, Suqian People's Hospital of Nanjing Drum Tower Hospital Group, Suqian, Jiangsu 223800, P.R. China.
Nanjing Drum Tower Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NORAD (non‑coding RNA activated by DNA damage) is a long non‑coding RNA (lncRNA) that is upregulated and promotes cell progression in various human types of cancer; however, its function in non‑small cell lung cancer (NSCLC) remains unclear. The present study investigated the regulatory function and underlying mechanisms of NORAD in NSCLC. NORAD and miR‑136‑5p expression were assessed by reverse transcription‑quantitative polymerase chain reaction, and proliferation and glycolysis‑associated markers were also assessed. Direct miR‑136‑5p regulation by NORAD was detected using luciferase reporter assay and RNA immunoprecipitation. NORAD was highly expressed in NSCLC tissues and cell lines. NORAD overexpression increased NSCLC proliferation and glycolysis. Further investigation revealed that NORAD serves as a competing endogenous RNA for miR‑136‑5p. Gain‑ and loss‑of‑function experiments confirmed that miR‑136‑5p reversed the promoting effects of NORAD in NSCLC. Results of the present study indicate that NORAD serves as a growth‑promoting lncRNA in NSCLC by suppressing the function of miR‑136‑5p. NORAD and miR‑136‑5p interaction may provide a potential target for NSCLC treatment.

Indexed as

Cell ProliferationAntagomirsBase SequenceCarcinoma, Non-Small-Cell LungCell Line, TumorE2F1 Transcription FactorGlycolysisHumansLung NeoplasmsMicroRNAsRNA InterferenceRNA, Long NoncodingRNA, Small InterferingSequence AlignmentAntagomirsE2F1 protein, humanE2F1 Transcription FactorMicroRNAsMIRN136 microRNA, humanNORAD long non-coding RNA, humanRNA, Long NoncodingRNA, Small Interfering

Identifiers

PMID31059060
PMCPMC6522956
OpenAlexW2942692373

What OpenQuestion 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 OpenQuestion graph.