Evidence map›Paper›PMID 30597845›Full record

ArticleMolecules (Basel, Switzerland)2018

MHY440, a Novel Topoisomerase Ι Inhibitor, Induces Cell Cycle Arrest and Apoptosis via a ROS-Dependent DNA Damage Signaling Pathway in AGS Human Gastric Cancer Cells.

Jung Yoon Jang, Yong Jung Kang, Bokyung Sung, Min Jeong Kim, Chaeun Park, Dongwan Kang, Hyung Ryong Moon, Hae Young Chung, Nam Deuk Kim

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 33 citations in OpenAlex.

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  17. Design and Synthesis of Novel Heterocyclic-Based 4Molecules (Basel, Switzerland) · 2019
    Article
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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 1 institution in 1 country.

Jung Yoon JangCollege of Pharmacy, Molecular Inflammation Research Center for Aging Intervention (MRCA), Pusan National University, Busan 46241, Korea. jungyoon486@hanmail.net.
Yong Jung KangCollege of Pharmacy, Molecular Inflammation Research Center for Aging Intervention (MRCA), Pusan National University, Busan 46241, Korea. biogreen80@hotmail.com.
Bokyung SungCollege of Pharmacy, Molecular Inflammation Research Center for Aging Intervention (MRCA), Pusan National University, Busan 46241, Korea. auvers1516@gmail.com.
Min Jeong KimCollege of Pharmacy, Molecular Inflammation Research Center for Aging Intervention (MRCA), Pusan National University, Busan 46241, Korea. nanum105@hanmail.net.
Chaeun ParkCollege of Pharmacy, Molecular Inflammation Research Center for Aging Intervention (MRCA), Pusan National University, Busan 46241, Korea. sauryyyy@pusan.ac.kr.
Dongwan KangCollege of Pharmacy, Molecular Inflammation Research Center for Aging Intervention (MRCA), Pusan National University, Busan 46241, Korea. 3607@pusan.ac.kr.
Hyung Ryong MoonCollege of Pharmacy, Molecular Inflammation Research Center for Aging Intervention (MRCA), Pusan National University, Busan 46241, Korea. mhr108@pusan.ac.kr.ORCID 0000-0003-1119-7112
Hae Young ChungCollege of Pharmacy, Molecular Inflammation Research Center for Aging Intervention (MRCA), Pusan National University, Busan 46241, Korea. hyjung@pusan.ac.kr.
Nam Deuk KimCollege of Pharmacy, Molecular Inflammation Research Center for Aging Intervention (MRCA), Pusan National University, Busan 46241, Korea. nadkim@pusan.ac.kr.ORCID 0000-0001-9033-9865
Pusan National University · KR

Funding

National Research Foundation of Korea 2009-0083538National Research Foundation of Korea 2018R1D1A1B07044648
6 · The paper itself

Abstract

We investigated the antitumor activity and action mechanism of MHY440 in AGS human gastric cancer cells. MHY440 inhibited topoisomerase (Topo) Ι activity and was associated with a DNA damage response signaling pathway. It exhibited a stronger anti-proliferative effect on AGS cells relative to Hs27 human foreskin fibroblast cells, and this effect was both time- and concentration-dependent. MHY440 also increased cell arrest in the G2/M phase by decreasing cyclin B1, Cdc2, and Cdc25c, and upregulating p53 and p73. MHY440 induced AGS cell apoptosis through the upregulation of Fas-L, Fas, and Bax as well as the proteolysis of BH3 interacting-domain death agonist and poly(ADP-ribose) polymerase. It also contributed to the loss of mitochondrial membrane potential. The apoptotic cell death induced by MHY440 was inhibited by pretreatment with Z-VAD-FMK, a pan-caspase inhibitor, indicating that apoptosis was caspase-dependent. Moreover, the apoptotic effect of MHY440 was reactive oxygen species (ROS)-dependent, as evidenced by the inhibition of MHY440-induced PARP cleavage and ROS generation via

Indexed as

DNA DamageApoptosisCaspasesCell Cycle CheckpointsCell Line, TumorEnzyme ActivationHumansMembrane Potential, MitochondrialModels, MolecularMolecular ConformationMolecular StructureProtein BindingReactive Oxygen SpeciesSignal TransductionStomach NeoplasmsStructure-Activity RelationshipCaspasesReactive Oxygen SpeciesTopoisomerase I Inhibitorsapoptosiscell cycle arrestgastric cancer cellsMHY440topoisomerase inhibitor

Identifiers

PMID30597845
PMCPMC6337620
OpenAlexW2907486571

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.