Evidence map›Paper›PMID 26919094›Full record

ArticleOncotarget2016

Selective killing of gastric cancer cells by a small molecule via targeting TrxR1 and ROS-mediated ER stress activation.

Weiqian Chen, Peng Zou, Zhongwei Zhao, Qiaoyou Weng, Xi Chen, Shilong Ying, Qingqing Ye, Zhe Wang, Jiansong Ji, Guang Liang

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

25 citing papers in PubMed, 53 citations in OpenAlex.

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  10. Therapeutic potential of curcumin in diabetic retinopathy (Review).International journal of molecular medicine · 2021
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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

10 authors at 2 institutions in 1 country.

Weiqian ChenChemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Peng ZouChemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Zhongwei ZhaoDepartment of Interventional Radiology, The Fifth Affiliated Hospital of Wenzhou Medical University, Lishui, Zhejiang, 323000, China.
Qiaoyou WengDepartment of Interventional Radiology, The Fifth Affiliated Hospital of Wenzhou Medical University, Lishui, Zhejiang, 323000, China.
Xi ChenChemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Shilong YingChemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Qingqing YeChemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Zhe WangChemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Jiansong JiDepartment of Interventional Radiology, The Fifth Affiliated Hospital of Wenzhou Medical University, Lishui, Zhejiang, 323000, China.
Guang LiangChemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Wenzhou Medical University · CNNanjing University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The thioredoxin reductase (TrxR) 1 is often overexpressed in numerous cancer cells. Targeting TrxR1 leads to a reduction in tumor progression and metastasis, making the enzyme an attractive target for cancer treatment. Our previous research revealed that the curcumin derivative B19 could induce cancer cell apoptosis via activation of endoplasmic reticulum (ER) stress. However, the upstream mechanism and molecular target of B19 is still unclear. In this study, we demonstrate that B19 directly inhibits TrxR1 enzyme activity to elevate oxidative stress and then induce ROS-mediated ER Stress and mitochondrial dysfunction, subsequently resulting in cell cycle arrest and apoptosis in human gastric cancer cells. A computer-assistant docking showed that B19 may bind TrxR1 protein via formation of a covalent bond with the residue Cys-498. Blockage of ROS production totally reversed B19-induced anti-cancer actions. In addition, the results of xenograft experiments in mice were highly consistent with in vitro studies. Taken together, targeting TrxR1 with B19 provides deep insight into the understanding of how B19 exerts its anticancer effects. More importantly, this work indicates that targeting TrxR1 and manipulating ROS levels are effective therapeutic strategy for the treatment of gastric cancer.

Indexed as

AnimalsApoptosisBlotting, WesternCell Cycle CheckpointsCell Line, TumorCurcuminEndoplasmic Reticulum StressHumansMembrane Potential, MitochondrialMice, Inbred BALB CMice, NudeReactive Oxygen SpeciesRNA InterferenceSmall Molecule LibrariesStomach NeoplasmsThioredoxin Reductase 1CurcuminReactive Oxygen SpeciesSmall Molecule LibrariesThioredoxin Reductase 1TXNRD1 protein, humanER stressgastric cancermitochondrial dysfunctionreactive oxygen species (ROS)thioredoxin reductase 1

Identifiers

PMID26919094
PMCPMC4941337
OpenAlexW2316022797

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.