Evidence map›Paper›PMID 30572915›Full record

ArticleJournal of experimental & clinical cancer research : CR2018

Arsenic trioxide reverses the chemoresistance in hepatocellular carcinoma: a targeted intervention of 14-3-3η/NF-κB feedback loop.

Yongxin Qiu, Yi Dai, Chi Zhang, Ye Yang, Ming Jin, Wenqi Shan, Jian Shen, Ming Lu, Zhaoyang Tang, Liang Ju and 9 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

27 citing papers in PubMed, 48 citations in OpenAlex.

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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

19 authors at 3 institutions in 2 countries.

Yongxin QiuThe Second Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Yi DaiJiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Jiangsu Collaborative Innovation Center For Cancer Personalized Medicine, School of Public Health, Nanjing Medical University, Nanjing, China.
Chi ZhangThe Second Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Ye YangJiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Jiangsu Collaborative Innovation Center For Cancer Personalized Medicine, School of Public Health, Nanjing Medical University, Nanjing, China.
Ming JinJiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Jiangsu Collaborative Innovation Center For Cancer Personalized Medicine, School of Public Health, Nanjing Medical University, Nanjing, China.
Wenqi ShanJiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Jiangsu Collaborative Innovation Center For Cancer Personalized Medicine, School of Public Health, Nanjing Medical University, Nanjing, China.
Jian ShenThe Second Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Ming LuThe Second Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Zhaoyang TangThe Second Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Liang JuThe Second Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Yuting WangJiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Jiangsu Collaborative Innovation Center For Cancer Personalized Medicine, School of Public Health, Nanjing Medical University, Nanjing, China.
Ruonan JiaoJiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Jiangsu Collaborative Innovation Center For Cancer Personalized Medicine, School of Public Health, Nanjing Medical University, Nanjing, China.
Yunwei XiaJiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Jiangsu Collaborative Innovation Center For Cancer Personalized Medicine, School of Public Health, Nanjing Medical University, Nanjing, China.
Guangming HuangThe Second Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Lihua YangThe Second Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Yuan LiJiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Jiangsu Collaborative Innovation Center For Cancer Personalized Medicine, School of Public Health, Nanjing Medical University, Nanjing, China. liyuan@njmu.edu.cn.
Jianping ZhangThe Second Affiliated Hospital of Nanjing Medical University, Nanjing, China. zjpnjmu@aliyun.com.
Vincent Kam Wai WongState Key Laboratory of Quality Research in Chinese Medicine, Macau Institute for Applied Research in Medicine and Health, Macau University of Science and Technology, Macau, China. kawwong@must.edu.mo.
Zhihong JiangState Key Laboratory of Quality Research in Chinese Medicine, Macau Institute for Applied Research in Medicine and Health, Macau University of Science and Technology, Macau, China. zhjiang@must.edu.mo.
Second Affiliated Hospital of Nanjing Medical University · CNNanjing Medical University · CNMacau University of Science and Technology · MO

Funding

National Natural Science Foundation of China 81572325National Natural Science Foundation of China 81602841National Natural Science Foundation of China 81874058Natural Science Foundation of Jiangsu Province BK20161570Project Funded by Jiangsu Collaborative Innovation Center For Cancer Personalized Medicine JX21817902/006
6 · The paper itself

Abstract

backgroundMulti-drug resistance (MDR) is one of the main obstacles for treatment of advanced/recurrent hepatocellular carcinoma (HCC). We have previously identified arsenic trioxide (ATO) as an effective metastasis/angiogenesis inhibitor in HCC. Here, we further found that MDR-HCC cells were more sensitive to ATO.

methodsThe MDR-HCC cells were used as experimental models. Biological functions were investigated using cell transfection, polymerase chain reaction, western blot, southwestern blot, immunostaining, immunoprecipitation plus atomic fluorescence spectrometry, and so on.

resultsThe MDR-HCC cells underwent high oxidative stress condition, and employed adaptive mechanisms for them to survive; while ATO abolished such mechanisms via targeting the 14-3-3η/nuclear factor kappa B (NF-κB) feedback Loop. Briefly, in MDR cells, the increase of ROS activated NF-κB signaling, which transcriptionally activated 14-3-3η. Meanwhile, the activation of NF-κB can be constitutively maintained by 14-3-3η. As a NF-κB inhibitor, ATO transcriptionally inhibited the 14-3-3η mRNA level. Meanwhile, ATO was also validated to directly bind to 14-3-3η, enhancing the degradation of 14-3-3η protein in an ubiquitination-dependent manner. Knockdown of 14-3-3η reduced the ATO-induced reversal extents of drug resistance in MDR cells.

conclusion14-3-3η/NF-κB feedback loop plays an important role in maintaining the MDR phenotype in HCC. Moreover, via targeting such feedback loop, ATO could be considered as a potential molecular targeted agent for the treatment of HCC.

Indexed as

14-3-3 ProteinsArsenic TrioxideCarcinoma, HepatocellularCell Line, TumorDrug Resistance, NeoplasmFeedback, PhysiologicalHumansLiver NeoplasmsNF-kappa BSignal TransductionTransfection14-3-3 ProteinsArsenic TrioxideNF-kappa BYWHAE protein, human14–3-3ηArsenic trioxideHepatocellular carcinomaMulti-drug resistanceNuclear factor kappa B

Identifiers

PMID30572915
PMCPMC6302299
OpenAlexW2904155716

What OpenQuestion holds

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LicenceCC BY
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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.