Evidence map›Paper›PMID 25013761›Full record

ArticleBioMed research international2014

p53 is a key regulator for osthole-triggered cancer pathogenesis.

Ssu-Ming Huang, Cheng-Fang Tsai, Dar-Ren Chen, Min-Ying Wang, Wei-Lan Yeh

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.4field-weighted citation impact, top 14% 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

10 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
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  8. Review
  9. Article
  10. Effect of Cnidium Lactone on Serum Mutant P53 and BCL-2/BAX Expression in Human Prostate Cancer Cells PC-3 Tumor-Bearing BALB/C Nude Mouse Model.Medical science monitor : international medical journal of experimental and clinical research · 2015
    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

5 authors at 3 institutions in 1 country.

Ssu-Ming HuangGraduate Institute of Biotechnology, National Chung Hsing University, Taichung 402, Taiwan ; Preventive Medicine Center, Department of Community Medicine, Taichung Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Taichung 427, Taiwan ; Division of Colon and Rectal Surgery, Department of Surgery, Taichung Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Taichung 427, Taiwan ; School of Medicine, Tzu Chi University, Hualien 970, Taiwan.
Cheng-Fang TsaiDepartment of Biotechnology, Asia University, Taichung 413, Taiwan.
Dar-Ren ChenComprehensive Breast Cancer Center, Changhua Christian Hospital, Changhua 500, Taiwan.ORCID 0000-0002-0897-4374
Min-Ying WangGraduate Institute of Biotechnology, National Chung Hsing University, Taichung 402, Taiwan.
Wei-Lan YehDepartment of Cell and Tissue Engineering, Changhua Christian Hospital, Changhua 500, Taiwan.ORCID 0000-0003-4398-7610
Changhua Christian Hospital · TWNational Chung Hsing University · TWAsia University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osthole has been reported to have antitumor activities via the induction of apoptosis and inhibition of cancer cell growth and metastasis. However, the detailed molecular mechanisms underlying the anticancer effects of osthole in human colon cancer remain unclear. In the present study, we have assessed osthole-induced cell death in two different human colon cancer cell lines, HCT116 and SW480. Our results also showed that osthole activated proapoptotic signaling pathways in human colon cancer cells. By using cell culture insert system, osthole reduced cell motility in both human colon cancer cell lines. This study also provides evidence supporting the potential of osthole in p53 activation. Expression of p53, an apoptotic protein, was remarkably upregulated in cells treated with osthole. Importantly, the levels of phosphorylation of p53 on Ser15 (p-p53) and acetylation of p53 on Lys379 (acetyl-p53) were increased under osthole treatment. Our results also demonstrated that p53 was activated followed by generation of reactive oxygen species (ROS) and activation of c-Jun N-terminal kinase (JNK). Our study provides novel insights of p53-mediated responses under osthole treatment. Taken together, we concluded that osthole induces cancer cell death and inhibits migratory activity in a controlled manner and is a promising candidate for antitumor drug development.

Indexed as

ApoptosisCell ProliferationCoumarinsGene Expression Regulation, NeoplasticHCT116 CellsHumansMAP Kinase Kinase 4Reactive Oxygen SpeciesTumor Suppressor Protein p53CoumarinsMAP Kinase Kinase 4ostholReactive Oxygen SpeciesTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID25013761
PMCPMC4075183
OpenAlexW2167687672

What OpenQuestion holds

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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.