Evidence map›Paper›PMID 28537893›Full record

ArticleOncotarget2017

Alpha-mangostin induces apoptosis through activation of reactive oxygen species and ASK1/p38 signaling pathway in cervical cancer cells.

Chien-Hsing Lee, Tsung-Ho Ying, Hui-Ling Chiou, Shu-Ching Hsieh, Shiua-Hua Wen, Ruey-Hwang Chou, Yi-Hsien Hsieh

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
13.2field-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

47 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. [Research progress on the pathogenesis and clinical treatment of cirrhotic cardiomyopathy].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026
    Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article
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

7 authors at 4 institutions in 1 country.

Chien-Hsing LeeSchool of Chinese Medicine, College of Chinese Medicine, China Medical University, Taichung, Taiwan.
Tsung-Ho YingDepartment of Obstetrics and Gynecology, Chung Shan Medical University Hospital, Taichung, Taiwan.
Hui-Ling ChiouSchool of Medical Laboratory and Biotechnology, Chung Shan Medical University, Taichung, Taiwan.
Shu-Ching HsiehSchool of Medical Laboratory and Biotechnology, Chung Shan Medical University, Taichung, Taiwan.
Shiua-Hua WenInstitute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, Taiwan.
Ruey-Hwang ChouGraduate Institute of Biomedical Sciences and Center for Molecular Medicine, China Medical University, Taichung, Taiwan.
Yi-Hsien HsiehInstitute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, Taiwan.
Chung Shan Medical University · TWAsia University · TWChina Medical University · TWChung Shan Medical University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alpha-mangostin, a natural xanthonoid, has been reported to possess the anti-cancer property in various types of human cancer. However, its effects and mechanism of α-mangostin in cervical cancer remain unclear. We found that α-mangostin effectively inhibited cell viability, resulted in loss of mitochondrial membrane potential (MMP), release of cytochrome C, increase of Bax, decrease of Bcl-2, and activation of caspase-9/caspase-3 cascade in cervical cancer cells. Alpha-mangostin elevated the contents of reactive oxygen species (ROS) to activate p38. Disrupting ASK1/p38 signaling pathway by a specific inhibitor of p38, or by the siRNAs against ASK1, MKK3/6, or p38, significantly abolished α-mangostin-induced cell death and apoptotic responses. Moreover, α-mangostin also repressed tumor growth in accordance with increased levels of p-ASK1, p-p38, cleaved-PARP and cleaved-caspase-3 in the tumor mass from the mouse xenograft model of cervical cancer. In the current study, we provided first evidence to demonstrate that dietary antioxidant α-mangostin could inhibit the tumor growth of cervical cancer cells through enhancing ROS amounts to activate ASK1/p38 signaling pathway and damage the integrity of mitochondria and thereby induction of apoptosis in cervical cancer cells.

Indexed as

AnimalsAntineoplastic AgentsApoptosisBreast NeoplasmsCell Line, TumorCytochromes cDisease Models, AnimalFemaleHumansMAP Kinase Kinase Kinase 5Matrix MetalloproteinasesMembrane Potential, MitochondrialMiceMitochondriaModels, Biologicalp38 Mitogen-Activated Protein KinasesAntineoplastic AgentsCytochromes cmangostinMAP Kinase Kinase Kinase 5Matrix Metalloproteinasesp38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsReactive Oxygen SpeciesXanthonesapoptosiscervical cancerp38MAPKreactive oxygen speciesα-mangostin

Identifiers

PMID28537893
PMCPMC5564576
OpenAlexW2612677677

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.