Evidence map›Paper›PMID 39792166›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2025

Coptisine inhibits esophageal carcinoma growth by modulating pyroptosis via inhibition of HGF/c-Met signaling.

Chunmei Qian, Xing Zhang, Yu-Shi Tian, Lin Yuan, Qiao Wei, Yifu Yang, Midie Xu, Xiaoyu Wang, Menghong Sun

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In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

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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

2 citing papers in PubMed.

  1. Review
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4 · The record

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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

9 authors.

Chunmei QianExperiment Center for Science and Technology, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.
Xing ZhangExperiment Center for Science and Technology, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.
Yu-Shi TianGraduate School of Pharmaceutical Sciences, Osaka University, Osaka, 565-0871, Japan.
Lin YuanExperiment Center for Science and Technology, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.
Qiao WeiDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Yifu YangExperiment Center for Science and Technology, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.
Midie XuDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China. xumd27202003@sina.com.
Xiaoyu WangExperiment Center for Science and Technology, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China. 0000002733@shutcm.edu.cn.
Menghong SunDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China. menghongs@163.com.

Funding

Traditional Chinese Medicine Science and Technology Development Project of Shanghai Medical Innovation & Development Foundation WL-HBQN-2022011K
6 · The paper itself

Abstract

Esophageal carcinoma is a highly prevalent malignancy worldwide. The present study aimed to investigate the mechanism by which the natural compound coptisine affects pyroptosis in esophageal squamous cell carcinoma (ESCC). The expression of c-Met in ESCC patients was assessed by immunohistochemical analysis of tissue microarrays. Natural drugs that bind to c-Met were identified by screening and molecular docking. The effect of coptisine on the proliferation of ESCC cells was detected by CCK-8 and colony formation assays. Cell cycle progression and cell apoptosis were detected by flow cytometry. The levels of mRNAs related to pyroptosis and miR-21 after coptisine treatment were assessed via real-time quantitative PCR. The effect of pyroptosis was evaluated by reactive oxygen species level detection and transmission electron microscopy (TEM) analysis. The expression of proteins related to pyroptosis and the HGF/c-Met pathway was detected by western blotting. A xenograft tumor model was established, and the inhibitory effect of coptisine was evaluated by observing tumor growth. The results showed that the highly expressed protein c-Met in esophageal cancer could bind with coptisine. Coptisine inhibited c-Met phosphorylation and proliferation in ESCC cells. Furthermore, coptisine inhibited the expression of downstream proteins of the HGF/c-Met signaling pathway and induced ROS generation. Tumor xenograft experiments demonstrated that coptisine effectively inhibited tumor growth by reducing the levels of pyroptosis-associated proteins. In conclusion, these findings indicate that inhibition of the HGF/c-Met signaling pathway suppresses pyroptosis to enhance the antitumor effect of coptisine in ESCC and support the potential use of coptisine for EC treatment.

Indexed as

Antineoplastic AgentsBerberineEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaHepatocyte Growth FactorProto-Oncogene Proteins c-metPyroptosisAnimalsCell Line, TumorCell ProliferationFemaleHumansMaleMiceMice, Inbred BALB CMice, NudeAntineoplastic AgentsBerberinecoptisineHepatocyte Growth FactorHGF protein, humanMET protein, humanProto-Oncogene Proteins c-metReactive Oxygen SpeciesCaspase-1CoptisineEsophageal squamous cell carcinomaHGF/c-MetPyroptosisROS

Identifiers

PMID39792166

What OpenQuestion holds

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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.