Evidence map›Paper›PMID 31488218›Full record

ArticleJournal of hematology & oncology2019

LINC01123, a c-Myc-activated long non-coding RNA, promotes proliferation and aerobic glycolysis of non-small cell lung cancer through miR-199a-5p/c-Myc axis.

Qian Hua, Mingming Jin, Baoming Mi, Fei Xu, Tian Li, Li Zhao, Jianjun Liu, Gang Huang

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Journal of hematology & oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 173 papers.

0numbers the graph read from it
0cells of the map it votes in
173citing papers in PubMed
13.4field-weighted citation impact, top 1% 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

173 citing papers in PubMed, 294 citations in OpenAlex.

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  17. Feasibility and mechanism ofAnnals of nuclear medicine · 2025
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  20. [Ferroptosis-related long non-coding RNA to predict the clinical outcome of non-small cell lung cancer after radiotherapy].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2025
    Article

113 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Qian HuaDepartment of Nuclear Medicine, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, 200127, China.
Mingming JinShanghai Key Laboratory of Molecular Imaging, Shanghai University of Medicine and Health Sciences, Shanghai, 201318, China.
Baoming MiDepartment of Nuclear Medicine, Affiliated Hospital of Jiangnan University (Wuxi 4th People's Hospital), Wuxi, 214062, Jiangsu, China.
Fei XuDepartment of Nuclear Medicine, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, 200127, China.
Tian LiShanghai Key Laboratory of Molecular Imaging, Shanghai University of Medicine and Health Sciences, Shanghai, 201318, China.
Li ZhaoDepartment of Nuclear Medicine, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, 200127, China.
Jianjun LiuDepartment of Nuclear Medicine, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, 200127, China. nuclearj@163.com.
Gang HuangDepartment of Nuclear Medicine, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, 200127, China. huanggang@sumhs.edu.cn.
Renji Hospital · CNShanghai University of Medicine and Health Sciences · CNWuxi Fourth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLong non-coding RNAs (lncRNAs) have been associated with non-small cell lung cancer (NSCLC), but the underlying molecular mechanisms of their specific roles in mediating aerobic glycolysis have been poorly explored.

methodsNext-generation RNA sequencing assay was performed to identify the differentially expressed RNAs between NSCLC tissues with high

resultsThree hundred sixty-four differentially expressed genes were identified in RNA-seq assay, and LINC01123 was one of the most overexpressed lncRNAs. Further validation in expanded NSCLC cohorts confirmed that LINC01123 was upregulated in 92 paired NSCLC tissues and associated with poor survival. Functional assays showed that LINC01123 promoted NSCLC cell proliferation and aerobic glycolysis. Mechanistic investigations revealed that LINC01123 was a direct transcriptional target of c-Myc. Meanwhile, LINC01123 increased c-Myc mRNA expression by sponging miR-199a-5p. In addition, rescue experiments showed that LINC01123 functioned as an oncogene depending on miR-199a-5p and c-Myc.

conclusionSince LINC01123 is upregulated in NSCLC, correlates with prognosis, and controls proliferation and aerobic glycolysis by a positive feedback loop with c-Myc, it is expected to be a potential biomarker and therapeutic target for NSCLC.

Indexed as

AnimalsCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationCohort StudiesGlycolysisHeterograftsHumansLung NeoplasmsMaleMiceMice, Inbred BALB CMice, NudeMicroRNAsPrognosisProto-Oncogene Proteins c-mycMicroRNAsmirn199 microRNA, humanMYC protein, humanProto-Oncogene Proteins c-mycRNA, Long Noncodingaerobic glycolysisc-MycLINC01123Long non-coding RNAsnon-small cell lung cancer

Identifiers

PMID31488218
PMCPMC6728969
OpenAlexW2971469357

What OpenQuestion holds

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LicenceCC BY
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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.