Evidence map›Paper›PMID 22139441›Full record

ArticleCarcinogenesis2012

Quercetin-3-methyl ether suppresses proliferation of mouse epidermal JB6 P+ cells by targeting ERKs.

Jixia Li, Madhusoodanan Mottamal, Haitao Li, Kangdong Liu, Feng Zhu, Yong-Yeon Cho, Carlos P Sosa, Keyuan Zhou, G Tim Bowden, Ann M Bode and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2012. 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
0.7field-weighted citation impact, top 35% 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, 34 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Neuroprotective Assessment ofPlants (Basel, Switzerland) · 2021
    Article
  5. Bioassay-guided Isolation of Flavonoids fromIranian journal of pharmaceutical research : IJPR · 2021
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
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

11 authors at 5 institutions in 2 countries.

Jixia LiThe Hormel Institute, University of Minnesota, Austin, MN 55912, USA.
Madhusoodanan Mottamal
Haitao Li
Kangdong Liu
Feng Zhu
Yong-Yeon Cho
Carlos P Sosa
Keyuan Zhou
G Tim Bowden
Ann M Bode
Zigang Dong
Hormel (United States) · USGuangdong Medical College · CNUniversity of Minnesota · USIBM (United States) · USUniversity of Arizona Cancer Center

Funding

VITAMIN A, AND ITS PRECURSORS AND DERIVATIVES AS THERAPEUTIC MODALITIESP01CA027502 · NCI · UNIVERSITY OF ARIZONA · PI EINSPAHR, JANINE G · 1985 to 2015
$36.3M
The role of histone phosphorylation in arsenic-induced cell transformation and skR01ES016548 · NIEHS · UNIVERSITY OF MINNESOTA · PI DONG, ZIGANG · 2008 to 2012
$1.7M
Anticarcinogenic Mechanisms of Tea ConstituentsR37CA081064 · NCI · UNIVERSITY OF MINNESOTA · PI DONG, ZIGANG · 2008 to 2012
$1.5M
Inhibition of Carcinogenesis by Tea and Tea ConstituentsR01CA120388 · NCI · UNIVERSITY OF MINNESOTA · PI DONG, ZIGANG · 2006 to 2010
$1.3M
NCI NIH HHS CA0120388NCI NIH HHS CA027502NCI NIH HHS P01 CA027502NCI NIH HHS R37CA081064NIEHS NIH HHS ES016548
6 · The paper itself

Abstract

Chemoprevention has been acknowledged as an important and practical strategy for the management of skin cancer. Quercetin-3-methyl ether, a naturally occurring compound present in various plants, has potent anticancer-promoting activity. We identified this compound by in silico virtual screening of the Traditional Chinese Medicine Database using extracellular signal-regulated kinase 2 (ERK2) as the target protein. Here, we showed that quercetin-3-methyl ether inhibited proliferation of mouse skin epidermal JB6 P+ cells in a dose- and time-dependent manner by inducing cell cycle G(2)-M phase accumulation. It also suppressed 12-O-tetradecanoylphorbol-13-acetate-induced neoplastic cell transformation in a dose-dependent manner. Its inhibitory effect was greater than quercetin. The activation of activator protein-1 was dose-dependently suppressed by quercetin-3-methyl ether treatment. Western blot and kinase assay data revealed that quercetin-3-methyl ether inhibited ERKs kinase activity and attenuated phosphorylation of ERKs. Pull-down assays revealed that quercetin-3-methyl ether directly binds with ERKs. Furthermore, a loss-of-function ERK2 mutation inhibited the effectiveness of the quercetin-3-methyl ether. Overall, these results indicated that quercetin-3-methyl ether exerts potent chemopreventive activity by targeting ERKs.

Indexed as

AnimalsCell CycleCell Cycle CheckpointsCell ProliferationCells, CulturedCell Transformation, NeoplasticChemopreventionEpidermal CellsEpidermisFlavonoidsMAP Kinase Signaling SystemMedicine, Chinese TraditionalMiceMitogen-Activated Protein Kinase 3MutationPhosphorylationFlavonoidsMitogen-Activated Protein Kinase 3Quercetinquercetin 3-O-methyl etherTranscription Factor AP-1

Identifiers

PMID22139441
PMCPMC3271267
OpenAlexW2158035471

What OpenQuestion holds

Textmetadata
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.