Evidence map›Paper›PMID 23913940›Full record

ArticleCarcinogenesis2014

The P110 subunit of PI3-K is a therapeutic target of acacetin in skin cancer.

Sung Keun Jung, Jong Eun Kim, Sung-Young Lee, Mee Hyun Lee, Sanguine Byun, Young A Kim, Tae Gyu Lim, Kanamata Reddy, Zunnan Huang, Ann M Bode and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

19 citing papers in PubMed, 40 citations in OpenAlex.

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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

13 authors at 2 institutions in 2 countries.

Sung Keun JungThe Hormel Institute, University of Minnesota, 801 16th Ave NE, Austin, MN 55912, USA.
Jong Eun Kim
Sung-Young Lee
Mee Hyun Lee
Sanguine Byun
Young A Kim
Tae Gyu Lim
Kanamata Reddy
Zunnan Huang
Ann M Bode
Hyong Joo Lee
Ki Won Lee
Zigang Dong
University of Minnesota · USSeoul National University · KR

Funding

Developing new ornithine decarboxylase inhibitors to prevent skin & colon cancerR01CA166011 · NCI · UNIVERSITY OF MINNESOTA · PI DONG, ZIGANG · 2013 to 2017
$1.6M
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
Molecular Mechanisms and Targets of Soy Compounds in the Prevention of Colon CancR21CA172457 · NCI · UNIVERSITY OF MINNESOTA · PI DONG, ZIGANG · 2013 to 2014
$327k
INSULIN AND STEROID INTERACTIONS IN BREAST CANCERR01CA016660 · NCI · UNIVERSITY OF ROCHESTER · PI HILF, RUSSELL · 1985 to 1998
–
NCI NIH HHS CA120388NCI NIH HHS CA1666011NCI NIH HHS CA172457NCI NIH HHS R01 CA166011NCI NIH HHS R21 CA172457NCI NIH HHS R37CA081064
6 · The paper itself

Abstract

The identification of primary molecular targets of cancer-preventive phytochemicals is essential for a comprehensive understanding of their mechanism of action. In the present study, we investigated the chemopreventive effects and molecular targets of acacetin, a flavonoid found in Robinia p seudoacacia, also known as black locust. Acacetin treatment significantly suppressed epidermal growth factor (EGF)-induced cell transformation. Immunoblot analysis revealed that acacetin attenuated EGF-induced phosphorylation of Akt and p70(S6K), which are downstream effectors of phosphatidylinositol 3-kinase (PI3-K). An immunoprecipitation kinase assay of PI3-K and pull-down assay results demonstrated that acacetin substantially inhibits PI3-K activity by direct physical binding. Acacetin exhibited stronger inhibitory effects against anchorage-dependent and -independent cell growth in cells expressing higher PI3-K activity compared with those exhibiting relatively low PI3-K activity. Binding assay data combined with computational modeling suggest that acacetin binds in an adenosine triphosphate (ATP)-competitive manner with the p110α subunit of PI3-K and interacts with Val828, Glu826, Asp911, Trp760, Ile777, Ile825, Tyr813, Ile910 and Met900 residues. Acacetin was also found to significantly reduce SK-MEL-28 tumor growth and Akt phosphorylation in vivo. Taken together, these results indicate that acacetin is an ATP-competitive PI3-K inhibitor and a promising agent for melanoma chemoprevention.

Indexed as

Phosphoinositide-3 Kinase InhibitorsAdenosine TriphosphateAnimalsAntineoplastic Agents, PhytogenicCell ProliferationCell Transformation, NeoplasticClass Ia Phosphatidylinositol 3-KinaseEnzyme InhibitorsEpidermal Growth FactorFlavonesMiceMice, NudeMolecular Docking SimulationPhosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene Proteins c-aktacacetinAdenosine TriphosphateAntineoplastic Agents, PhytogenicClass Ia Phosphatidylinositol 3-KinaseEnzyme InhibitorsEpidermal Growth FactorFlavonesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-akt

Identifiers

PMID23913940
PMCPMC3895936
OpenAlexW2166619670

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.