Evidence map›Paper›PMID 24525337›Full record

ArticleOncotarget2014

AKT mediates actinomycin D-induced p53 expression.

Chih-Shou Chen, Dong-Ru Ho, Fei-Yun Chen, Chang-Rong Chen, Yu-De Ke, Jyan-Gwo Joseph Su

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 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
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  5. Actinomycin D and bortezomib disrupt protein homeostasis in Wilms tumor.bioRxiv : the preprint server for biology · 2024
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  16. p53 induction and cell viability modulation by genotoxic individual chemicals and mixtures.Environmental science and pollution research international · 2018
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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

6 authors at 2 institutions in 1 country.

Chih-Shou ChenDivision of Urology, Department of Surgery, Chang Gung Memorial Hospital, Chiayi, Taiwan, ROC.
Dong-Ru Ho
Fei-Yun Chen
Chang-Rong Chen
Yu-De Ke
Jyan-Gwo Joseph Su
National Chiayi University · TWChiayi Chang Gung Memorial Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

At high cytotoxic concentrations, actinomycin D (ActD) blocks transcription, decreasing levels of MDM2 and thus causing p53 stabilization. At low cytostatic concentrations, ActD causes ribosomal stress, which decreases MDM2 activity, resulting in p53 stabilization and activation. ActD can thus be used for p53-based cyclotherapy. We analyzed pathways mediating ActD-induced p53 expression. Inhibitors (LY294002, wortmannin, and deguelin) of phosphatidylinositol 3-kinases (PI3K) and AKT, but not inhibitors of MEK1/2, JNK, and p38-MAPK abolished the ActD-induced p53 expression in diverse cell types. RNA interference further supported these results. When AKT was downregulated by small hairpin RNA-AKTs, ActD-induced p53 expression was significantly decreased. ActD caused AKT phosphorylation at Ser473, indicating full activation of AKT. The potential for cancer therapy is discussed.

Indexed as

ApoptosisDactinomycinDose-Response Relationship, DrugHEK293 CellsHep G2 CellsHumansPhosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene Proteins c-aktSignal TransductionTumor Suppressor Protein p53DactinomycinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID24525337
PMCPMC3996664
OpenAlexW1680776268

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.