Evidence map›Paper›PMID 24337632›Full record

ArticleOncology reports2014

Active form of AKT controls cell proliferation and response to apoptosis in hepatocellular carcinoma.

Imge Kunter, Esra Erdal, Deniz Nart, Funda Yilmaz, Sedat Karademir, Ozgul Sagol, Nese Atabey

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 19% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Pooled it
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  11. Anti-Hepatocellular Carcinoma Biomolecules: Molecular Targets Insights.International journal of molecular sciences · 2021
    Review
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  16. Extract Derived fromMolecules (Basel, Switzerland) · 2020
    Article
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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 2 institutions in 1 country.

Imge KunterDepartment of Medical Biology and Genetics, Faculty of Medicine, Dokuz Eylul University, Inciralti, Izmir 35340, Turkey.
Esra ErdalDepartment of Medical Biology and Genetics, Faculty of Medicine, Dokuz Eylul University, Inciralti, Izmir 35340, Turkey.
Deniz NartDepartment of Pathology, Faculty of Medicine, Ege University, Bornova, Izmir 35100, Turkey.
Funda YilmazDepartment of Pathology, Faculty of Medicine, Ege University, Bornova, Izmir 35100, Turkey.
Sedat KarademirDepartment of General Surgery, Faculty of Medicine, Dokuz Eylul University, Inciralti, Izmir 35340, Turkey.
Ozgul SagolDepartment of Pathology, Faculty of Medicine, Dokuz Eylul University, Inciralti, Izmir 35340, Turkey.
Nese AtabeyDepartment of Medical Biology and Genetics, Faculty of Medicine, Dokuz Eylul University, Inciralti, Izmir 35340, Turkey.
Dokuz Eylül University · TREge University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is the third most common cause of cancer-related mortality worldwide. Deregulation of the AKT signaling pathway has been found in HCC. However, the effect of AKT activation on the proliferation and apoptosis in HCC is not clear. Herein, expression of phosphorylated form of AKT (Ser 473) was investigated in HCC tumor (n=73), cirrhosis (n=17), normal liver (n=22) samples and in HCC cell lines (n=8). The results showed that expression of p-AKT was higher in tumor (53%) than in cirrhotic tissues (12%) while it was absent in normal liver (p<0.0001). p-AKT expression was also associated with number of tumor nodules and differentiation status (p<0.05). LY294002 induced cell cycle arrest at G0/G1 in SNU-449 and Mahlavu cells by decreasing expression of CDK2, CDK4, CycD1, CycD3, CycE, CycA and increasing expression of p21 and p27 as well; it also caused a decrease in the E2F1 transcriptional activity through declining phosphorylated Rb. LY294002 did not affect the basal level of apoptosis; however, it amplified cisplatin-induced apoptosis in SNU-449 cells. When the p-AKT level was decreased specifically after transfection with the DN-AKT plasmid, SNU-449 cells became more sensitive to cisplatin-induced apoptosis. HuH-7 cells with no basal p-AKT, were markedly affected by the treatment of doxorubicin. Thus, Akt signaling controls growth and chemical-induced apoptosis in HCC and p-AKT may be a potential target for therapeutic interventions in HCC patients.

Indexed as

Antineoplastic AgentsApoptosisCarcinoma, HepatocellularCell Line, TumorCell ProliferationChromonesCisplatinEnzyme ActivationEnzyme InhibitorsFemaleG1 Phase Cell Cycle CheckpointsHumansLiverLiver NeoplasmsMaleMorpholines2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneAntineoplastic AgentsChromonesCisplatinEnzyme InhibitorsMorpholinesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-akt

Identifiers

PMID24337632
PMCPMC3896502
OpenAlexW1975884367

What OpenQuestion holds

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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.