Evidence map›Paper›PMID 25874498›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2015

A Aconitum coreanum polysaccharide fraction induces apoptosis of hepatocellular carcinoma (HCC) cells via pituitary tumor transforming gene 1 (PTTG1)-mediated suppression of the P13K/Akt and activation of p38 MAPK signaling pathway and displays antitumor activity in vivo.

Ming Liang, Jianchao Liu, Hongyu Ji, Moyang Chen, Yonghua Zhao, Shuchen Li, Xiaoyu Zhang, Jingyuan Li

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Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.4field-weighted citation impact, top 7% 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

18 citing papers in PubMed, 33 citations in OpenAlex.

  1. iScience · 2026
    Article
  2. Article
  3. Article
  4. Review
  5. The protective effect and antitumor activity ofFrontiers in pharmacology · 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

8 authors at 2 institutions in 1 country.

Ming LiangDepartment of Infectious Diseases, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China. minglianghmu@126.com.
Jianchao LiuDepartment of Infectious Diseases, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Hongyu JiDepartment of Infectious Diseases, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Moyang ChenDepartment of Infectious Diseases, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Yonghua ZhaoDepartment of Infectious Diseases, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Shuchen LiDepartment of Infectious Diseases, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Xiaoyu ZhangDepartment of Infectious Diseases, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Jingyuan LiDepartment of Infectious Diseases, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Second Affiliated Hospital of Harbin Medical University · CNHarbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this study, we observed that a Aconitum coreanum polysaccharide (CACP) exhibited an effective inhibitory effect on H22 cell growth in vitro and in vivo via the induction of apoptosis. Further, quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting assays revealed that the expression of pituitary tumor transforming gene 1 (PTTG1), one proto-oncogene, was evidently suppressed in both transcript and protein levels in H22 cell model or mice after CACP treatment. Particularly, CACP (40 μg/ml) treatment or transfection with PTTG1 small interfering RNA (siRNA) could greatly reduce the phosphorylation of Akt (p-Akt) but increase phospho-p38 mitogen-activated protein kinase (p-p38 MARK) protein levels in H22 cells as compared with vehicle-treated cells. Likewise, following treatment of H22-tumor-bearing mice with CACP (100 mg/kg), doxorubicin (DOX, 3 mg/kg), and their combination, tumor tissues showed an attenuated p-Akt protein expression, but a striking p-p38 MARK level when compared with those in model mice. Taken together, we demonstrated here the inhibitory effect of CACP on the growth of H22 cells in vitro and in vivo, which may be through, at least partly, repression of PTTG1 and then followed by the inactivation of P13/Akt and activation of p38 MARK signaling pathways. These findings offered a novel approach for the treatment of hepatocellular carcinoma (HCC) in the future.

Indexed as

AconitumAnimalsApoptosisCarcinoma, HepatocellularCell ProliferationClass I Phosphatidylinositol 3-KinasesGene Expression Regulation, NeoplasticHumansLiver NeoplasmsMiceOncogene Protein v-aktp38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesPolysaccharidesProto-Oncogene MasSecurinClass I Phosphatidylinositol 3-KinasesMAS1 protein, humanOncogene Protein v-aktp38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesPik3cd protein, mousepituitary tumor-transforming protein 1, humanPolysaccharidesProto-Oncogene MasSecurinAconitum coreanumAntitumorP13K/Aktp38 MAPKPituitary tumor transforming gene 1 (PTTG1)Polysaccharides

Identifiers

PMID25874498
OpenAlexW2084503273

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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.