Evidence map›Paper›PMID 28927105›Full record

ArticleOncology letters2017

Reactive oxygen species-driven mitochondrial injury induces apoptosis by teroxirone in human non-small cell lung cancer cells.

Jing-Ping Wang, Chang-Heng Hsieh, Chun-Yen Liu, Kai-Han Lin, Pei-Tsun Wu, Kwun-Min Chen, Kang Fang

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

12 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
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  8. Polyphenolic Fraction Obtained FromFrontiers in pharmacology · 2020
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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

7 authors at 1 institution in 1 country.

Jing-Ping WangDepartment of Life Science, National Taiwan Normal University, Taipei 116, Taiwan, R.O.C.
Chang-Heng HsiehDepartment of Life Science, National Taiwan Normal University, Taipei 116, Taiwan, R.O.C.
Chun-Yen LiuDepartment of Life Science, National Taiwan Normal University, Taipei 116, Taiwan, R.O.C.
Kai-Han LinDepartment of Life Science, National Taiwan Normal University, Taipei 116, Taiwan, R.O.C.
Pei-Tsun WuDepartment of Life Science, National Taiwan Normal University, Taipei 116, Taiwan, R.O.C.
Kwun-Min ChenDepartment of Chemistry, National Taiwan Normal University, Taipei 116, Taiwan, R.O.C.
Kang FangDepartment of Life Science, National Taiwan Normal University, Taipei 116, Taiwan, R.O.C.
National Taiwan Normal University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Teroxirone as an anticancer agent is used to treat human lung cancer by inducing apoptotic cell death. Previous studies have demonstrated that the status of the tumor suppressor p53 determined the onset of apoptotic cell death in human non-small cell lung cancer cells (NSCLC). In order to further understand the underlying mechanisms of lung cancer, the present study explored the targets of teroxirone. By including antioxidants, the present study analyzed changes in cell proliferation, cell cycle division, mitochondrial membrane potential (MMP), reactive oxygen species (ROS), expression of apoptosis markers and cytochrome

Indexed as

apoptosismitochondriareactive oxygen speciesteroxirone

Identifiers

PMID28927105
PMCPMC5588047
OpenAlexW2734341876

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.