Evidence map›Paper›PMID 25638174›Full record

ArticleJournal of translational medicine2015

Luteolin exerts a marked antitumor effect in cMet-overexpressing patient-derived tumor xenograft models of gastric cancer.

Jun Lu, Guangliang Li, Kuifeng He, Weiqin Jiang, Cong Xu, Zhongqi Li, Haohao Wang, Weibin Wang, Haiyong Wang, Xiaodong Teng and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
6.6field-weighted citation impact, top 2% 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

40 citing papers in PubMed, 71 citations in OpenAlex.

  1. Review
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  6. Potential anticancer effects and toxicity of flavones luteolin and apigeninJournal of environmental science and health. Part C, Toxicology and carcinogenesis · 2025
    Review
  7. Review
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  9. Article
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  11. Anti-Tumor Effects and Toxicity Reduction Mechanisms ofMolecules (Basel, Switzerland) · 2024
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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 1 institution in 1 country.

Jun LuDepartment of Surgical Oncology, The 1st Affiliated Hospital, School of Medicine, Zhejiang University, NO. 79 Qingchun Road, Hangzhou, 310003, Zhejiang, China. weedses@hotmail.com.
Guangliang LiDepartment of Surgical Oncology, The 1st Affiliated Hospital, School of Medicine, Zhejiang University, NO. 79 Qingchun Road, Hangzhou, 310003, Zhejiang, China. fans_1988@163.com.
Kuifeng HeDepartment of Surgical Oncology, The 1st Affiliated Hospital, School of Medicine, Zhejiang University, NO. 79 Qingchun Road, Hangzhou, 310003, Zhejiang, China. hekfeng@aliyun.com.
Weiqin JiangDepartment of Surgical Oncology, The 1st Affiliated Hospital, School of Medicine, Zhejiang University, NO. 79 Qingchun Road, Hangzhou, 310003, Zhejiang, China. 15068117618@163.com.
Cong XuDepartment of Surgical Oncology, The 1st Affiliated Hospital, School of Medicine, Zhejiang University, NO. 79 Qingchun Road, Hangzhou, 310003, Zhejiang, China. 18858283440@126.com.
Zhongqi LiDepartment of Surgical Oncology, The 1st Affiliated Hospital, School of Medicine, Zhejiang University, NO. 79 Qingchun Road, Hangzhou, 310003, Zhejiang, China. yuqing@zju.edu.cn.
Haohao WangDepartment of Surgical Oncology, The 1st Affiliated Hospital, School of Medicine, Zhejiang University, NO. 79 Qingchun Road, Hangzhou, 310003, Zhejiang, China. coldhot33@163.com.
Weibin WangDepartment of Surgical Oncology, The 1st Affiliated Hospital, School of Medicine, Zhejiang University, NO. 79 Qingchun Road, Hangzhou, 310003, Zhejiang, China. wb_wang@126.com.
Haiyong WangDepartment of Surgical Oncology, The 1st Affiliated Hospital, School of Medicine, Zhejiang University, NO. 79 Qingchun Road, Hangzhou, 310003, Zhejiang, China. hywang98@gmail.com.
Xiaodong TengDepartment of Pathology, The 1st Affiliated Hospital, School of Medicine, Zhejiang University, NO. 79 Qingchun Road, Hangzhou, 310003, Zhejiang, China. 339251158@qq.com.
Lisong TengDepartment of Surgical Oncology, The 1st Affiliated Hospital, School of Medicine, Zhejiang University, NO. 79 Qingchun Road, Hangzhou, 310003, Zhejiang, China. 11218203@zju.edu.cn.
Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAberrated activation of cMet in gastric cancer contributes to tumor growth, angiogenesis and metastasis. cMet-overexpressing gastric cancer has a poor prognosis because of high tumor metastasis and limited therapeutic options. Luteolin is a common dietary flavonoid with antitumor properties. However, the antitumor effect of luteolin on cMet-overexpressing gastric cancer remain unclear.

methodsTwo cMet-overexpressing patient-derived human tumor xenograft (PDTX) models of gastric cancer were established, and treated with luteolin or vehicle to evaluate the antitumor effects of luteolin. Tumor specimens were subjected to H&E staining and immunohistochemistry. MKN45 and SGC7901 cells that show high cMet expression were treated with varying concentrations of luteolin and evaluated by western blot, cell viability, apoptosis, migration, and invasion assays.

resultsLuteolin inhibited the tumor growth in cMet-overexpressing PDTX models. Immunohistochemistry demonstrated that expression of cMet, MMP9 and Ki-67 were significantly down-regulated. Luteolin inhibited proliferation, promoted apoptosis and reduced the invasiveness of MKN45 and SGC7901 cells. Western blot revealed that luteolin promoted the activation of apoptosis-related proteins, caspase-3 and PARP-1, and down-regulated the invasion-associated protein, MMP9. Further studies demonstrated that luteolin decreased the expression and phosphorylation of cMet, and downstream phosphorylation of Akt and ERK. In addition, luteolin down-regulated phosphorylated Akt independently of cMet. Blocking Akt and/or ERK with the PI3K inhibitor, LY294002, or the ERK inhibitor, PD98059, induced down-regulation of MMP9 and up-regulation of cleaved caspase-3 and PARP-1, resembling the effects of luteolin.

conclusionsOur findings ,for the first time, demonstrate that luteolin exerts marked antitumor effects in cMet-overexpressing PDTX models of gastric cancer, through a mechanism likely involving cMet/Akt/ERK signaling. These findings indicate that luteolin may act as a potential therapeutic option for cMet-overexpressing gastric cancer.

Indexed as

Xenograft Model Antitumor AssaysAnimalsAntineoplastic AgentsCell Line, TumorCell MovementCell ProliferationDown-RegulationFemaleHumansImmunoblottingLuteolinMice, Inbred BALB CMice, NudeNeoplasm InvasivenessNeoplasm ProteinsProto-Oncogene Proteins c-metAntineoplastic AgentsLuteolinNeoplasm ProteinsProto-Oncogene Proteins c-met

Identifiers

PMID25638174
PMCPMC4320638
OpenAlexW2165593729

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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.