Evidence map›Paper›PMID 26401077›Full record

ArticleWorld journal of gastroenterology2015

Mechanism of QHF-cisplatin against hepatocellular carcinoma in a mouse model.

Tao Chen, Shen-Jun Yuan, Jing Wang, Wei Hu

Open access · hybridAbstract readComparative Study
In one paragraph

Article in World journal of gastroenterology, 2015. 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
0.2field-weighted citation impact, top 44% 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

2 citing papers in PubMed, 8 citations in OpenAlex.

  1. Bioactive Products Targeting C-Met As Potential Antitumour Drugs.Anti-cancer agents in medicinal chemistry · 2025
    Review
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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

4 authors at 1 institution in 1 country.

Tao ChenTao Chen, Wei Hu, the Third Level of TCM Pharmacology Research Laboratory affiliated to China TCM Administration, Medical Science College of China Three Gorges University, Yichang 443002, Hubei Province, China.
Shen-Jun YuanTao Chen, Wei Hu, the Third Level of TCM Pharmacology Research Laboratory affiliated to China TCM Administration, Medical Science College of China Three Gorges University, Yichang 443002, Hubei Province, China.
Jing WangTao Chen, Wei Hu, the Third Level of TCM Pharmacology Research Laboratory affiliated to China TCM Administration, Medical Science College of China Three Gorges University, Yichang 443002, Hubei Province, China.
Wei HuTao Chen, Wei Hu, the Third Level of TCM Pharmacology Research Laboratory affiliated to China TCM Administration, Medical Science College of China Three Gorges University, Yichang 443002, Hubei Province, China.
China Three Gorges University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo study the effects of QHF-cisplatin on H22 hepatocellular carcinoma (HCC) and their mechanisms of action.

methodsSixty BALB/c mice were randomly divided into a model group (n = 48) and a normal control group (n = 12). An HCC xenograft tumor was created by injecting H22 cells directly into the liver parenchyma of the mice. The 48 BALB/c mice in the model group were randomly divided into four groups: QHF, DDP (cisplatin), QHF plus DDP, and model control. The inhibitory effects of these drugs on tumor growth were evaluated by calculating the rate of tumor growth inhibition. The mice were examined by observing their general condition, body weight and survival time. Changes in tumor tissue were observed under an optical microscope. Aspartate aminotransferase (AST), alanine aminotransferase (ALT) and α-fetoprotein (AFP) levels in serum were measured. Hepatocyte growth factor (HGF), c-mesenchymal-epithelial transition (c-Met) factor, phosphorylated (p)-c-Met, p38, p-p38, extracellular signal-regulated kinase (ERK), p-ERK and vascular endothelial growth factor (VEGF) levels were evaluated in tumor and liver tissues using western blotting.

resultsCompared with the DDP group, a lower incidence of toxic reactions and a higher survival time were observed in the QHF plus DDP group. Tumor weight was significantly lower in the QHF, DDP and QHF plus DDP groups than in the model control group (0.24 ± 0.07, 0.18 ± 0.03 and 0.14 ± 0.01 g vs 0.38 ± 0.05 g, respectively), and the differences were statistically significant (P < 0.01). The rate of tumor growth inhibition in the QHF, DDP and QHF plus DDP groups was 38.7%, 52.6% and 63.5%, respectively. AST, ALT and AFP levels in serum were significantly lower in the QHF, DDP and QHF plus DDP groups compared to the model control group (P < 0.05). Similarly, HGF, p-c-Met, p-p38, p-ERK and VEGF levels in tumor tissue were significantly lower in the QHF, DDP and QHF plus DDP groups (P < 0.05).

conclusionQHF and DDP have an antiangiogenic effect on H22 HCC in mice. QHF inhibits tumor growth via blocking the HGF/c-Met signaling pathway, inhibiting p38, ERK and VEGF signaling.

Indexed as

Angiogenesis InhibitorsAnimalsAntineoplastic Combined Chemotherapy ProtocolsBiomarkers, TumorCarcinoma, HepatocellularCell Line, TumorCisplatinDrugs, Chinese HerbalEpithelial-Mesenchymal TransitionFemaleLiver Neoplasms, ExperimentalMaleMice, Inbred BALB CSignal TransductionTime FactorsTumor BurdenAngiogenesis InhibitorsBiomarkers, TumorCisplatinDrugs, Chinese HerbalCisplatinc-MetH22 cellsHepatocellular carcinomaHepatocyte growth factorQHF formula

Identifiers

PMID26401077
PMCPMC4572793
OpenAlexW2415586607

What OpenQuestion holds

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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.