Evidence map›Paper›PMID 30518397›Full record

ArticleJournal of experimental & clinical cancer research : CR2018

The natural polyphenol curcumin induces apoptosis by suppressing STAT3 signaling in esophageal squamous cell carcinoma.

Ying Liu, Xinhua Wang, Shuang Zeng, Xiane Zhang, Jimin Zhao, Xiaoyan Zhang, Xinhuan Chen, Wanjing Yang, Yili Yang, Ziming Dong and 3 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 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
3.9field-weighted citation impact, top 4% 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

54 citing papers in PubMed, 99 citations in OpenAlex.

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  20. Hypolipidemic and Anti-Inflammatory Effects ofInternational journal of molecular sciences · 2023
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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

13 authors at 3 institutions in 1 country.

Ying LiuDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, 450001, People's Republic of China.
Xinhua WangDepartment of Histology and Embryology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, 450001, People's Republic of China.
Shuang ZengDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, 450001, People's Republic of China.
Xiane ZhangDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, 450001, People's Republic of China.
Jimin ZhaoDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, 450001, People's Republic of China.
Xiaoyan ZhangDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, 450001, People's Republic of China.
Xinhuan ChenDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, 450001, People's Republic of China.
Wanjing YangDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, 450001, People's Republic of China.
Yili YangSuzhou Institute of Systems Medicine, Center for Systems Medicine, Chinese Academy of Medical Sciences, Suzhou, Jiangsu, 215123, People's Republic of China.
Ziming DongDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, 450001, People's Republic of China.
Jingyu ZhuSchool of Medicine and Pharmaceutics, Jiangnan University, Wuxi, Jiangsu, 214000, People's Republic of China.
Xin XuDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, 450001, People's Republic of China. zitanxu@163.com.ORCID http://orcid.org/0000-0001-7713-4734
Fang TianDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, 450001, People's Republic of China. tianfang418@163.com.
Zhengzhou University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNJiangnan University · CN

Funding

Foundation and Frontier Technology Research Project in Henan Province 142300410325National Natural Sciences Foundation of China U1304813Natural Science Foundation of Jiangsu Province BK20171231the Science Foundation of the Henan Province of China 17A310032Young Teacher Special Fund of Zhengzhou University 1421328055
6 · The paper itself

Abstract

backgroundWe and others have previously shown that the STAT3 signaling pathway is activated in some esophageal squamous cell carcinoma (ESCC) cells and is required for the survival and growth of these primary ESCC-derived xenografts. It has also been shown that the natural polyphenol curcumin is an effective anti-tumor agent.

methodsLuciferase assay and immunoblotting were performed to examine whether curcumin suppressed STAT3 signaling. CCK-8 assay and xenografts were utilized for analyzing ESCC cell growth in culture and mice. Soft agar assay was carried out to determine the colony formation ability of ESCC cells in the presence or absence of curcumin. Cell death and cell cycle were assessed by In CELL Analyzer 2000. Immunohistochemistry and TUNEL assay were used for detecting apoptosis in ESCC tisuses. Molecular docking was performed to evaluate the interaction of curcumin with JAK2. JAK2 activity was assessed using an in vitro cell-free system. HE staining was used to evaluate the ESCC tissues.

resultsThe natural polyphenol curcumin inhibited STAT3 phosphorylation rapidly and blocked STAT3-mediated signaling in ESCC cells. It also induced growth arrest and apoptosis in cultured ESCC cells, which were attenuated by enforced expression of STAT3. Furthermore, curcumin preferentially blocked the growth of primary ESCC-derived xenografts that harbored activated STAT3.

conclusionsCurcumin is able to exert anti-tumor action through inhibiting the STAT3 signaling pathway. Giving its wide use in traditional medicines with low toxicity and few adverse reactions, it is conceivable that curcumin might be further explored as a unique STAT3 inhibitor for anti-cancer therapies.

Indexed as

AnimalsApoptosisCell Line, TumorCurcuminEsophageal Squamous Cell CarcinomaFemaleHumansMiceMice, SCIDMolecular Docking SimulationSignal TransductionSTAT3 Transcription FactorSurvival AnalysisTransfectionXenograft Model Antitumor AssaysCurcuminSTAT3 protein, humanSTAT3 Transcription FactorApoptosisCurcuminEsophageal squamous cell carcinomaPDX modelSTAT3

Identifiers

PMID30518397
PMCPMC6280482
OpenAlexW2902977814

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.