Evidence map›Paper›PMID 31819483›Full record

ArticleOncoTargets and therapy2019

THUMPD3-AS1 Is Correlated With Non-Small Cell Lung Cancer And Regulates Self-Renewal Through miR-543 And ONECUT2.

Jia Hu, Youfang Chen, Xiaodong Li, Huikai Miao, Rongzhen Li, Dongni Chen, Zhesheng Wen

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

23 citing papers in PubMed, 38 citations in OpenAlex.

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  10. Pan-cancer analysis identifiesTranslational cancer research · 2022
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  19. Emerging role of ONECUT2 in tumors.Oncology letters · 2020
    Review
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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

7 authors at 2 institutions in 1 country.

Jia HuDepartment of Thoracic Oncology, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou 510060, People's Republic of China.
Youfang ChenDepartment of Thoracic Oncology, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou 510060, People's Republic of China.
Xiaodong LiDepartment of Thoracic Oncology, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou 510060, People's Republic of China.
Huikai MiaoDepartment of Thoracic Oncology, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou 510060, People's Republic of China.
Rongzhen LiDepartment of Thoracic Oncology, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou 510060, People's Republic of China.
Dongni ChenDepartment of Thoracic Oncology, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou 510060, People's Republic of China.
Zhesheng WenDepartment of Thoracic Oncology, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou 510060, People's Republic of China.
Sun Yat-sen University Cancer Center · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOf all malignancies, lung cancer is the leading cause of death, and non-small cell lung cancer (NSCLC) accounts for 80-85% of all lung cancers. In this study, the long non-coding RNA (lncRNA) THUMPD3-AS1 was observed to be highly expressed in NSCLC and correlated with TNM stages and relapse, suggesting that THUMPD3-AS1 is involved in the regulation of NSCLC.

methodsThe aim of this study was to investigate the regulatory function and mechanism of THUMPD3-AS1 in NSCLC cells by cellular function and molecular biology experiments.

resultsOverexpression and knockdown analysis revealed that THUMPD3-AS1 promoted tumor progression by increasing cell proliferation and self-renewal of NSCLC cells. Moreover, THUMPD3-AS1 may act as an endogenous sponge of microRNA-543 (miR-543) which can regulate the target gene ONECUT2 in NSCLC cells.

conclusionOur study indicated that THUMPD3-AS1 regulated NSCLC cell self-renewal by regulating the expression of miR-543 and ONECUT2, and THUMPD3-AS1 can potentially act as a biomarker or therapeutic target in NSCLC.

Indexed as

miR-543non-small cell lung cancerONECUT2self-renewalTHUMPD3-AS1

Identifiers

PMID31819483
PMCPMC6875498
OpenAlexW2985677016

What OpenQuestion holds

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LicenceCC BY-NC
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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.