Evidence map›Paper›PMID 30833546›Full record

ArticleCell death & disease2019

Decrease of AIM2 mediated by luteolin contributes to non-small cell lung cancer treatment.

Qian Yu, Minda Zhang, Qidi Ying, Xin Xie, Shuwen Yue, Bending Tong, Qing Wei, Zhaoshi Bai, Lingman Ma

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

48 citing papers in PubMed, 98 citations in OpenAlex.

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  16. New prospects of cancer therapy based on pyroptosis and pyroptosis inducers.Apoptosis : an international journal on programmed cell death · 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.

Qian YuState Key Laboratory of Natural Medicines, School of Life Science and Technology, China Pharmaceutical University, Nanjing, 210009, Jiangsu, China.
Minda ZhangState Key Laboratory of Natural Medicines, Department of Physiology, China Pharmaceutical University, Nanjing, 210009, Jiangsu, China.
Qidi YingDepartment of Pharmacology, School of Pharmacy, China Pharmaceutical University, Nanjing, 210009, Jiangsu, China.
Xin XieState Key Laboratory of Natural Medicines, School of Life Science and Technology, China Pharmaceutical University, Nanjing, 210009, Jiangsu, China.
Shuwen YueDepartment of Pharmacology, School of Pharmacy, China Pharmaceutical University, Nanjing, 210009, Jiangsu, China.
Bending TongJiangsu Cancer Hospital & Jiangsu Institute of Cancer Research & The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, 210009, Jiangsu, China.
Qing WeiJiangsu Cancer Hospital & Jiangsu Institute of Cancer Research & The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, 210009, Jiangsu, China.
Zhaoshi BaiJiangsu Cancer Hospital & Jiangsu Institute of Cancer Research & The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, 210009, Jiangsu, China. baizhaoshi23@126.com.
Lingman MaState Key Laboratory of Natural Medicines, School of Life Science and Technology, China Pharmaceutical University, Nanjing, 210009, Jiangsu, China. 1620174416@cpu.edu.cn.
China Pharmaceutical University · CNJiangsu Cancer Hospital · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-small cell lung cancer (NSCLC) is one of the most common malignancies in the world. Although extensive studies showed that luteolin exhibited antitumor effects against NSCLC, the mechanism has not been fully established. In the present study, we found that luteolin significantly reduced the expression of absent in melanoma 2 (AIM2) at both mRNA and protein levels leading to the suppression of AIM2 inflammasome activation, which induced G2/M phase arrest and inhibited epithelial-mesenchymal transition (EMT) in NSCLC. Furthermore, the inhibitory effects of luteolin on NSCLC cells were abolished by the knockdown of AIM2. On the contrary, the antitumor effects of luteolin could be notably reversed by the overexpression of AIM2. In addition, luteolin reduced poly(dA:dT)-induced caspase-1 activation and IL-1β cleavage in NSCLC cells. These findings suggested that AIM2 was essential to luteolin-mediated antitumor effects. The antitumor effects of luteolin, which were closely associated with AIM2, were also confirmed in the A549 and H460 xenograft mouse models. Collectively, our study displayed that the antitumor effects of luteolin on NSCLC were AIM2 dependent and the downregulation of AIM2 might be an effective way for NSCLC treatment.

Indexed as

AnimalsCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationDNA-Binding ProteinsEpithelial-Mesenchymal TransitionG2 Phase Cell Cycle CheckpointsGene Expression Regulation, NeoplasticHeterograftsHumansInflammasomesLuteolinMaleMice, Inbred BALB CMice, NudeAIM2 protein, humanDNA-Binding ProteinsInflammasomesLuteolin

Identifiers

PMID30833546
PMCPMC6399355
OpenAlexW2919382176

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.