Evidence map›Paper›PMID 24553354›Full record

ArticleOncotarget2014

Hydrogen peroxide/ATR-Chk2 activation mediates p53 protein stabilization and anti-cancer activity of cheliensisin A in human cancer cells.

Jingjie Zhang, Guangxun Gao, Liang Chen, Jingxia Li, Xu Deng, Qin-shi Zhao, Chuanshu Huang

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.5field-weighted citation impact, top 16% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Hydroxypropyl-Frontiers 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 3 institutions in 2 countries.

Jingjie ZhangNelson Institute of Environmental Medicine, New York University School of Medicine, Tuxedo, NY, USA;
Guangxun Gao
Liang Chen
Jingxia Li
Xu Deng
Qin-shi Zhao
Chuanshu Huang
New York University · USKunming Institute of Botany · CNAir Force Medical University · CN

Funding

Vaccine FacilityP30CA016087 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ADRIANA HEGUY · 1985 to 2026
$83.1M
RESEARCH IN ENVIRONMENTAL HEALTH SCIENCES (CENTER GRANT)P30ES000260 · NIEHS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI COSTA, MAX · 1985 to 2020
$26.1M
Reagent/Service CoreP01CA165980 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI WU, XUE-RU · 2013 to 2023
$13.5M
Molecular Mechanisms of Nickel-Induced TumorigenicityR01CA112557 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI HUANG, CHUANSHU · 2004 to 2016
$2.9M
Mechanisms underlying therapeutic effect of a new compound Isorhapontigenin (ISO)R01CA177665 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI HUANG, CHUANSHU · 2013 to 2018
$1.7M
NCI NIH HHS CA165980NCI NIH HHS P01 CA165980NCI NIH HHS P30 CA016087NCI NIH HHS R01 CA112557NCI NIH HHS R01 CA177665NIEHS NIH HHS ES000260NIEHS NIH HHS P30 ES000260
6 · The paper itself

Abstract

Chiliensisine A (Chel A) as a novel styryl-lactone isolated from Goniothalamus cheliensis Hu has been indicated to be a chemotherapeutic agent in Leukemia HL-60 cells. However, its potential for cancer treatment and the underlying mechanisms are not deeply investigated to the best of our knowledge. Current studies showed that Chel A could trigger p53-mediated apoptosis, accompanied with dramatically inhibition of anchorage-independent growth of human colon cancer HCT116 cells. Further studies found that Chel A treatment resulted in p53 protein stabilization and accumulation via the induction of its phosphorylation at Ser20 and Ser15. Moreover, Chel A-induced p53 protein accumulation and activation required ATR/Chk2 axis, which is distinct from the mechanism that we have most recently identified the Chk1/p53-dependent apoptotic response by Chel A in normal mouse epidermal Cl41 cells. In addition, our results demonstrated that hydrogen peroxide generation induced by Chel A acted as a precursor for all these signaling events and downstream biological effects. Taken together, we have identified the Chel A as a new therapeutic agent, which highlights its potential for cancer therapeutic effect.

Indexed as

ApoptosisAtaxia Telangiectasia Mutated ProteinsCheckpoint Kinase 2Colonic NeoplasmsEpoxy CompoundsHCT116 CellsHumansHydrogen PeroxidePyronesSignal TransductionTransfectionTumor Suppressor Protein p53Tumor Suppressor ProteinsAtaxia Telangiectasia Mutated ProteinsATR protein, humanCheckpoint Kinase 2CHEK2 protein, humancheliensisin AEpoxy CompoundsHydrogen PeroxidePyronesTP53 protein, humanTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID24553354
PMCPMC3996661
OpenAlexW2170958992

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.