Evidence map›Paper›PMID 32958825›Full record

ArticleBritish journal of cancer2020

CB11, a novel purine-based PPARɣ ligand, overcomes radio-resistance by regulating ATM signalling and EMT in human non-small-cell lung cancer cells.

Tae Woo Kim, Da-Won Hong, Joung Whan Park, Sung Hee Hong

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

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  10. Nuclear Receptors and Lipid Sensing.Advances in experimental medicine and biology · 2022
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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

4 authors at 2 institutions in 1 country.

Tae Woo KimDivision of Radiation Biomedical Research, Korea Institute of Radiological and Medical Sciences, Seoul, 139-706, Republic of Korea.
Da-Won HongLaboratory of RNA Cell Biology, Graduate Department of Bioconvergence Science and Technology, Dankook University, Jukjeon-ro 152, Suji-gu, Yongin-si, Gyeonggi-do, 16892, Republic of Korea.
Joung Whan ParkDivision of Radiation Biomedical Research, Korea Institute of Radiological and Medical Sciences, Seoul, 139-706, Republic of Korea.
Sung Hee HongDivision of Radiation Biomedical Research, Korea Institute of Radiological and Medical Sciences, Seoul, 139-706, Republic of Korea. gobrian@kcch.re.kr.
Korea Institute of Radiological and Medical Sciences · KRDankook University · KR

Funding

National Research Foundation of Korea (NRF) No.2017 R1D1A1B03033922
6 · The paper itself

Abstract

backgroundPeroxisome proliferator-activated receptor γ (PPARγ) agonists frequently induce cell death in human non-small-cell lung cancer (NSCLC) cells. However, majority of NSCLC patients acquire resistance after cancer therapy, and it is still unclear.

methodsIn this study we investigated the apoptotic mechanism and the anti-cancer effects of a novel purine-based PPARγ agonist, CB11 (8-(2-aminophenyl)-3-butyl-1,6,7-trimethyl-1H-imidazo[2,1-f]purine-2,4(3H,8H)-dione), on human NSCLC cells. CB11 mediates PPARγ-dependent cell death, reactive oxygen species (ROS) production, mitochondrial membrane potential (MMP) collapse, cell cycle arrest, lactate dehydrogenase (LDH) cytotoxicity, and caspase-3 activity in human NSCLC cells.

resultsCB11 causes cell death via ROS-mediated ATM-p53-GADD45α signalling in human NSCLC cells, and diphenyleneiodonium (DPI), an NADPH oxidase inhibitor, decreases cell death by inhibiting CB11-mediated ATM signalling. In a xenograft experiment, CB11 dramatically reduced tumour volume when compared to a control group. Furthermore, CB11 induced cell death by inhibiting epithelial-to-mesenchymal transition (EMT) under radiation exposure in radiation-resistant human NSCLC cells. However, PPARγ deficiency inhibited cell death by blocking the ATM-p53 axis in radiation/CB11-induced radiation-resistant human NSCLC cells.

conclusionsTaken together, our results suggest that CB11, a novel PPARγ agonist, may be a novel anti-cancer agent, and it could be useful in a therapeutic strategy to overcome radio-resistance in radiation-exposed NSCLC.

Indexed as

3T3 CellsAdipocytesAnilidesAnimalsApoptosisAtaxia Telangiectasia Mutated ProteinsAzo CompoundsCarcinoma, Non-Small-Cell LungCaspase 3Caspase 9Cell Cycle CheckpointsCell Cycle ProteinsCell DeathCell DifferentiationCell Line, TumorDNA Damage2-chloro-5-nitrobenzanilide8-(2-aminophenyl)-3-butyl-1,6,7-trimethyl-1H-imidazo(2,1-f)purine-2,4(3H,8H)-dioneAnilidesAtaxia Telangiectasia Mutated ProteinsAzo CompoundsCaspase 3Caspase 9Cell Cycle ProteinsciglitazonediphenyleneiodoniumGADD45A protein, humanGADD45 ProteinsImidazolesLigandsL-Lactate DehydrogenaseLuciferasesoil red OOnium CompoundsPPAR gammaPurinesReactive Oxygen SpeciesRNA, Small InterferingThiazolidinedionesTumor Suppressor Protein p53

Identifiers

PMID32958825
PMCPMC7723055
OpenAlexW3087395632

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.