Evidence map›Paper›PMID 30825105›Full record

ArticleInvestigational new drugs2019

A high-throughput drug screen identifies auranofin as a potential sensitizer of cisplatin in small cell lung cancer.

Xiaoli Liu, Wei Wang, Yanping Yin, Ming Li, Hong Li, Hang Xiang, Ao Xu, Xiaodong Mei, Bo Hong, Wenchu Lin

Abstract read
PubMed Publisher
In one paragraph

Article in Investigational new drugs, 2019. 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
1.5field-weighted citation impact, top 16% 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, 27 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

10 authors at 2 institutions in 1 country.

Xiaoli LiuHigh Magnetic Field Laboratory, Chinese Academy of Sciences, Hefei, 230031, Anhui, People's Republic of China.
Wei WangHigh Magnetic Field Laboratory, Chinese Academy of Sciences, Hefei, 230031, Anhui, People's Republic of China.
Yanping YinHigh Magnetic Field Laboratory, Chinese Academy of Sciences, Hefei, 230031, Anhui, People's Republic of China.
Ming LiHigh Magnetic Field Laboratory, Chinese Academy of Sciences, Hefei, 230031, Anhui, People's Republic of China.
Hong LiHigh Magnetic Field Laboratory, Chinese Academy of Sciences, Hefei, 230031, Anhui, People's Republic of China.
Hang XiangHigh Magnetic Field Laboratory, Chinese Academy of Sciences, Hefei, 230031, Anhui, People's Republic of China.
Ao XuThe First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230001, People's Republic of China.
Xiaodong MeiThe First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230001, People's Republic of China.
Bo HongHigh Magnetic Field Laboratory, Chinese Academy of Sciences, Hefei, 230031, Anhui, People's Republic of China. bhong@hmfl.ac.cn.ORCID http://orcid.org/0000-0001-8117-5029
Wenchu LinHigh Magnetic Field Laboratory, Chinese Academy of Sciences, Hefei, 230031, Anhui, People's Republic of China. wenchu@hmfl.ac.cn.
University of Science and Technology of China · CNChinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Small cell lung cancer (SCLC) is a highly lethal malignancy with the 5-year survival rate of less than 7%. Chemotherapy-resistance is a major challenge for SCLC treatment in clinic. In the study, we developed a high-throughput drug screen strategy to identify new drugs that can enhance the sensitivity of chemo-drug cisplatin in SCLC. This screen identified auranofin, a US Food and Drug Administration (FDA)-approved drug used therapeutically for rheumatoid arthritis, as a sensitizer of cisplatin. Further study validated that auranofin synergistically enhanced the anti-tumor activity of cisplatin in chemo-resistant SCLC cells, which was accompanied by the enhanced induction of cell cycle arrest and apoptosis. The synergistic action of auranofin and cisplatin was through ROS overproduction, thereby leading to mitochondrial dysfunction and DNA damage. Furthermore, in vivo study demonstrated that the combination treatment of auranofin and cisplatin dramatically inhibited tumor growth in SCLC. Therefore, our study provides a rational basis for further clinical study to test whether auranofin could enhance the sensitivity of cisplatin-based therapy in SCLC patients.

Indexed as

AnimalsAntineoplastic AgentsApoptosisAuranofinCell CycleCell Line, TumorCell SurvivalCisplatinDNA DamageDrug Screening Assays, AntitumorHigh-Throughput Screening AssaysHumansLung NeoplasmsMice, NudeMitochondriaReactive Oxygen SpeciesAntineoplastic AgentsAuranofinCisplatinReactive Oxygen SpeciesAuranofinCiplatinDNA damageROSSmall cell lung cancer

Identifiers

PMID30825105
OpenAlexW2920419627

What OpenQuestion holds

Textmetadata
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.