Evidence map›Paper›PMID 39028451›Full record

ArticleChinese journal of integrative medicine2025

Cinobufacini Inhibits Survival and Metastasis of Hepatocellular Carcinoma via c-Met Signaling Pathway.

Ya-Nan Ma, Xue-Mei Jiang, Xi-Qi Hu, Ling Wang, Jian-Jun Gao, Hui Liu, Fang-Hua Qi, Pei-Pei Song, Wei Tang

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Article in Chinese journal of integrative medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
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

9 authors.

Ya-Nan MaDepartment of Gastroenterology, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Haikou, 570311, China.
Xue-Mei JiangDepartment of Gastroenterology, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Haikou, 570311, China.
Xi-Qi HuCenter for Clinical Sciences, National Center for Global Health and Medicine, Tokyo, 162-8655, Japan.
Ling WangObstetrics and Gynecology Hospital, Fudan University, Shanghai, 200011, China.
Jian-Jun GaoDepartment of Pharmacology, School of Pharmacy, Qingdao University, Qingdao, Shandong Province, 266021, China.
Hui LiuCentral South University, Xiangya School of Medicine Affiliated Haikou Hospital, Haikou, 570208, China.
Fang-Hua QiTraditional Chinese Medicine, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, China. qifanghua2006@126.com.
Pei-Pei SongCenter for Clinical Sciences, National Center for Global Health and Medicine, Tokyo, 162-8655, Japan. psong@it.ncgm.go.jp.
Wei TangInternational Health Care Center, National Center for Global Health and Medicine, Tokyo, 162-8655, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate the anti-tumor effects of cinobufacini (CINO) on hepatocellular carcinoma (HCC) induced by des-gamma-carboxy-prothrombin (DCP) and to uncover the underlying mechanisms.

methodsThe inhibitory effect of CINO on HCC cell proliferation was evaluated using the cell counting kit-8 method, and the apoptosis rate was quantified using flow cytometry. Immunofluorescence and Western blot analyses were used to investigate the differential expression of proteins associated with cell growth, apoptosis, migration, and invasion pathways after CINO treatment. The therapeutic potential of CINO for HCC was confirmed, and the possibility of combining cinobufacini with c-Met inhibitor for the treatment of primary HCC was further validated by in vivo experiments.

resultsUnder the induction of DCP, CINO inhibited the activity of HCC cells, induced apoptosis, and inhibited migration and invasion. Upon the induction of DCP, CINO regulated c-Met activation and the activation of the phosphatidylinositol-3 kinase/protein kinase B (PI3K/AKT) and mitogen-activated protein kinase kinase/extracellular signal-regulated kinase (MEK/ERK) pathways. In a mouse model of HCC, CINO exhibited significant antitumor effects by inhibiting the phosphorylation of c-Met and the downstream PI3K/AKT and MEK/ERK pathways in tumor tissues.

conclusionsCINO inhibited HCC cell growth, promoted apoptosis, and suppressed HCC cell invasion and migration by targeting c-Met and PI3K/AKT and MEK/ERK signaling pathways under DCP induction.

Indexed as

Amphibian VenomsBufanolidesCarcinoma, HepatocellularLiver NeoplasmsProto-Oncogene Proteins c-metSignal TransductionAnimalsApoptosisBiomarkersCell Line, TumorCell MovementCell ProliferationCell SurvivalHumansMaleMiceacarboxyprothrombinAmphibian VenomsBiomarkersBufanolideshuachansuPhosphatidylinositol 3-KinasesProtein PrecursorsProthrombinProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-metChinese medicinecinobufacinic-Met signaling pathwaydes-gamma-carborxy-prothrombinhepatocellular carcinomasurvival

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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.