Evidence map›Paper›PMID 27126362›Full record

ArticleCancer letters2016

Activation of AKT negatively regulates the pro-apoptotic function of death-associated protein kinase 3 (DAPK3) in prostate cancer.

Trinath P Das, Suman Suman, A M Sashi Papu John, Deeksha Pal, Angelena Edwards, Houda Alatassi, Murali K Ankem, Chendil Damodaran

Open access · hybridAbstract read
In one paragraph

Article in Cancer letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.7field-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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Pooled it
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  12. Research Advances in the Role of the Tropomyosin Family in Cancer.International journal of molecular sciences · 2023
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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

8 authors at 1 institution in 1 country.

Trinath P DasDepartment of Urology, University of Louisville, Louisville, KY, USA.
Suman SumanDepartment of Urology, University of Louisville, Louisville, KY, USA.
A M Sashi Papu JohnDepartment of Urology, University of Louisville, Louisville, KY, USA.
Deeksha PalDepartment of Urology, University of Louisville, Louisville, KY, USA.
Angelena EdwardsDepartment of Urology, University of Louisville, Louisville, KY, USA.
Houda AlatassiDepartment of Pathology, University of Louisville, Louisville, KY, USA.
Murali K AnkemDepartment of Urology, University of Louisville, Louisville, KY, USA.
Chendil DamodaranDepartment of Urology, University of Louisville, Louisville, KY, USA. Electronic address: chendil.damodaran@louisville.edu.
University of Louisville · US

Funding

Targeting AR and Akt for the Treatment of Prostate CancerR01CA138797 · NCI · UNIVERSITY OF LOUISVILLE · PI DAMODARAN, CHENDIL · 2010 to 2015
$1.5M
Dietary prevention of prostate cancerR01CA140605 · NCI · UNIVERSITY OF LOUISVILLE · PI DAMODARAN, CHENDIL · 2010 to 2015
$1.5M
NCI NIH HHS R01 CA138797NCI NIH HHS R01 CA140605
6 · The paper itself

Abstract

The activation of AKT governs many signaling pathways and promotes cell growth and inhibits apoptosis in human malignancies including prostate cancer (CaP). Here, we investigated the molecular association between AKT activation and the function of death-associated protein kinase 3 (DAPK3) in CaP. An inverse correlation of pAKT and DAPK3 expression was seen in a panel of CaP cell lines. Inhibition of AKT by wortmannin/LY294002 or overexpression of DAPK3 reverts the proliferative function of AKT in CaP cells. On the other hand, ectopic expression of AKT inhibited DAPK3 function and induced proliferation of CaP cells. In addition, AKT over-expressed tumors exhibit aggressive growth when compared to control vector in xenograft models. The immunohistochemistry results revealed a down-regulation of DAPK3 expression in AKT over-expressed tumors as compared to control tumors. Finally, we examined the expression pattern of AKT and DAPK3 in human CaP specimens - the expected gradual increase and nuclear localization of pAKT was seen in higher Gleason score samples versus benign hyperplasia (BPH). On the contrary, reduced expression of DAPK3 was seen in higher Gleason stages versus BPH. This suggests that inhibition of DAPK3 may be a contributing factor to the carcinogenesis of the prostate. Understanding the mechanism by which AKT negatively regulates DAPK3 function may suggest whether DAPK3 can be a therapeutic target for CaP.

Indexed as

ApoptosisAnimalsCell Line, TumorCell ProliferationDeath-Associated Protein KinasesEnzyme ActivationHumansMaleMice, Inbred BALB CMice, NudeNeoplasm GradingPhosphorylationProstatic NeoplasmsProtein Kinase InhibitorsProto-Oncogene Proteins c-aktSignal TransductionDAPK3 protein, humanDeath-Associated Protein KinasesProtein Kinase InhibitorsProto-Oncogene Proteins c-aktMolecular signalingOncogeneProgressionProstate cancerTumor suppressor

Identifiers

PMID27126362
PMCPMC4884664
OpenAlexW2345206038

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.