Evidence map›Paper›PMID 34644678›Full record

ArticleAging2021

Potentiated lung adenocarcinoma (LUAD) cell growth, migration and invasion by lncRNA DARS-AS1 via miR-188-5p/ KLF12 axis.

Yangyang Liu, Lu Liang, Liang Ji, Fuquan Zhang, Donglai Chen, Shanzhou Duan, Hao Shen, Yao Liang, Yongbing Chen

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2021. 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
4.3field-weighted citation impact, top 4% 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, 48 citations in OpenAlex.

  1. Article
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  5. Tumor-promoting UBR4 coordinates impaired mitophagy-associated senescence and lung adenocarcinoma pathogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  13. Aging · 2024
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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 3 institutions in 1 country.

Yangyang LiuDepartment of Thoracic Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Lu LiangDepartment of General Surgery, The Affiliated Zhangjiagang Hospital of Soochow University, Suzhou, China.
Liang JiDepartment of General Surgery, The Affiliated Zhangjiagang Hospital of Soochow University, Suzhou, China.
Fuquan ZhangDepartment of Thoracic Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Donglai ChenDepartment of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University, School of Medicine, Shanghai, China.
Shanzhou DuanDepartment of Thoracic Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Hao ShenDepartment of General Surgery, The Affiliated Zhangjiagang Hospital of Soochow University, Suzhou, China.
Yao LiangDepartment of General Surgery, The Affiliated Zhangjiagang Hospital of Soochow University, Suzhou, China.
Yongbing ChenDepartment of Thoracic Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Soochow University · CNSecond Affiliated Hospital of Soochow University · CNShanghai Pulmonary Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung adenocarcinoma (LUAD) is the most common histological type of non-small cell lung cancer (NSCLC). Due to the nonspecific early symptoms, the majority of the diagnosed LUAD patients are in the middle and late stages, with multiple metastases, and have missed the optimal period for treatment. Current studies have reported lncRNA DARS-AS1 as a cancer-promoting gene that expedites tumorigenesis. This is the first study demonstrating that DARS-AS1 is involved in the mediating process of LUAD. Cell functional experiments revealed that lncRNA DARS-AS1 participated in enhancing LUAD proliferation, invasion, and migration by inhibiting miR-188-5p. The investigation on DARS-AS1/miR-188-5p led to the discovery of KLF12 as a downstream target of miR-188-5p, and the regulatory pathway was established as DARS-AS1/miR-188-5p/KLF12. According to western blot results, DARS-AS1 promoted LUAD cell growth, migration, and invasion via stimulation of the PI3K/AKT pathway, activating the EMT process, and up-regulating the CyclinD1 and Bcl-2 proteins. This was the first report on the DARS-AS1/miR-188-5p/KLF12 axis and offered a novel strategy for early diagnosis, a new therapeutic method, and an improved prognosis for LUAD.

Indexed as

Adenocarcinoma of LungLung NeoplasmsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansKruppel-Like Transcription FactorsMicroRNAsNeoplasm InvasivenessRNA, Long NoncodingKLF12 protein, humanKruppel-Like Transcription FactorsMicroRNAsMIRN188 microRNA, humanRNA, Long NoncodingDARS-AS1Krüppel-like factor 12lncRNAlung adenocarcinomamiR-188-5p

Identifiers

PMID34644678
PMCPMC8544313
OpenAlexW3207758269

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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.