Evidence map›Paper›PMID 34226508›Full record

ArticleCell death discovery2021

Cloperastine inhibits esophageal squamous cell carcinoma proliferation in vivo and in vitro by suppressing mitochondrial oxidative phosphorylation.

Bo Li, Yin Yu, Yanan Jiang, Lili Zhao, Ang Li, Mingzhu Li, Baoyin Yuan, Jing Lu, Ziming Dong, Jimin Zhao and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

12 citing papers in PubMed, 20 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

11 authors at 3 institutions in 1 country.

Bo Li *The Pathophysiology Department, School of Basic Medical Sciences, College of Medicine, Zhengzhou University, Zhengzhou, 450000, China.
Yin Yu *The Pathophysiology Department, School of Basic Medical Sciences, College of Medicine, Zhengzhou University, Zhengzhou, 450000, China.
Yanan Jiang *The Pathophysiology Department, School of Basic Medical Sciences, College of Medicine, Zhengzhou University, Zhengzhou, 450000, China.
Lili ZhaoThe Pathophysiology Department, School of Basic Medical Sciences, College of Medicine, Zhengzhou University, Zhengzhou, 450000, China.
Ang LiThe Pathophysiology Department, School of Basic Medical Sciences, College of Medicine, Zhengzhou University, Zhengzhou, 450000, China.
Mingzhu LiThe Pathophysiology Department, School of Basic Medical Sciences, College of Medicine, Zhengzhou University, Zhengzhou, 450000, China.
Baoyin YuanThe Pathophysiology Department, School of Basic Medical Sciences, College of Medicine, Zhengzhou University, Zhengzhou, 450000, China.
Jing LuThe Pathophysiology Department, School of Basic Medical Sciences, College of Medicine, Zhengzhou University, Zhengzhou, 450000, China.
Ziming DongThe Pathophysiology Department, School of Basic Medical Sciences, College of Medicine, Zhengzhou University, Zhengzhou, 450000, China.
Jimin ZhaoThe Pathophysiology Department, School of Basic Medical Sciences, College of Medicine, Zhengzhou University, Zhengzhou, 450000, China. zhaojimin@zzu.edu.cn.
Kangdong LiuThe Pathophysiology Department, School of Basic Medical Sciences, College of Medicine, Zhengzhou University, Zhengzhou, 450000, China. kdliu@zzu.edu.cn.
Zhengzhou University · CNChina-US (Henan) Hormel Cancer Institute · CNHenan Cancer Hospital · CN

Funding

Natural Science Foundation of Henan Province (Henan Province Natural Science Foundation) 161100510300
6 · The paper itself

Abstract

Esophageal squamous cell carcinoma (ESCC) is a major type of esophageal cancer. The prognosis of patients with ESCC remains poor because of the high morbidity and mortality of the disease. One strategy for drug discovery for ESCC treatment or prevention is screening FDA-approved drugs. In the present study, we found that the antitussive agent cloperastine can inhibit the proliferation of ESCC cells. However, the underlying mechanism was unclear. To determine the mechanism of this inhibitory effect, we performed proteomic analysis using KYSE150 cells treated with cloperastine and DMSO. The results identified several down-regulated signaling pathways included those of three key proteins (NADH dehydrogenase [ubiquinone] 1 alpha subcomplex 1, NADH ubiquinone oxidoreductase subunit S5, and cytochrome C oxidase subunit 6B1) involved in oxidative phosphorylation. Meanwhile, we observed that oxidative phosphorylation in mitochondria was inhibited by the drug. Importantly, cloperastine suppressed ESCC growth in a xenograft mouse model in vivo. Our findings revealed that cloperastine inhibits the proliferation of ESCC in vivo and in vitro by suppressing mitochondrial oxidative phosphorylation.

Identifiers

PMID34226508
PMCPMC8257628
OpenAlexW3181197099

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.