Evidence map›Paper›PMID 27533079›Full record

ArticleOncotarget2016

Akt isoform specific effects in ovarian cancer progression.

Nicolle M Linnerth-Petrik, Lisa A Santry, Roger Moorehead, Manfred Jücker, Sarah K Wootton, Jim Petrik

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.1field-weighted citation impact, top 8% 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, 47 citations in OpenAlex.

  1. International journal of molecular sciences · 2026
    Article
  2. Review
  3. AKT kinases as therapeutic targets.Journal of experimental & clinical cancer research : CR · 2024
    Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. AKT Isoforms as a Target in Cancer and Immunotherapy.Current topics in microbiology and immunology · 2022
    Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Targeting the PI3K/AKT/mTOR/NFκB Axis in Ovarian Cancer.Journal of cellular immunology · 2020
    Article
  20. Article
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 2 countries.

Nicolle M Linnerth-PetrikDepartment of Pathobiology, Ontario Veterinary College, University of Guelph, Guelph, ON, Canada.
Lisa A SantryDepartment of Pathobiology, Ontario Veterinary College, University of Guelph, Guelph, ON, Canada.
Roger MooreheadDepartment of Biomedical Sciences, Ontario Veterinary College, University of Guelph, Guelph, ON, Canada.
Manfred JückerCenter of Experimental Medicine, Institute of Biochemistry and Signal Transduction, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Sarah K WoottonDepartment of Pathobiology, Ontario Veterinary College, University of Guelph, Guelph, ON, Canada.
Jim PetrikDepartment of Biomedical Sciences, Ontario Veterinary College, University of Guelph, Guelph, ON, Canada.
University of Guelph · CAUniversity Medical Center Hamburg-Eppendorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ovarian cancer remains a significant therapeutic problem and novel, effective therapies are needed. Akt is a serine-threonine kinase that is overexpressed in numerous cancers, including ovarian. Mammalian cells express three Akt isoforms which are encoded by distinct genes. Although there are several Akt inhibitors in clinical trials, most indiscriminately target all isoforms. Current in vitro data and animal knockout experiments suggest that the Akt isoforms may have divergent roles. In this paper, we determined the isoform-specific functions of Akt in ovarian cancer cell proliferation in vitro and in ovarian cancer progression in vivo. For in vitro experiments, murine and human ovarian cancer cells were treated with Akt inhibitors and cell viability was assessed. We used two different in vivo approaches to identify the roles of Akt isoforms in ovarian cancer progression and their influence on the primary tumor and tumor microenvironment. In one experiment, wild-type C57Bl6 mice were orthotopically injected with ID8 cells with stable knockdown of Akt isoforms. In a separate experiment, mice null for Akt 1-3 were orthotopically injected with WT ID8 cells (Figure 1). Our data show that inhibition of Akt1 significantly reduced ovarian cancer cell proliferation and inhibited tumor progression in vivo. Conversely, disruption of Akt2 increased tumor growth. Inhibition of Akt3 had an intermediate phenotype, but also increased growth of ovarian cancer cells. These data suggest that there is minimal redundancy between the Akt isoforms in ovarian cancer progression. These findings have important implications in the design of Akt inhibitors for the effective treatment of ovarian cancer.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCell Line, TumorCell ProliferationCell SurvivalDisease Models, AnimalDisease ProgressionFemaleGene Knockdown TechniquesHumansMiceMice, KnockoutNeoplasm MetastasisOvarian NeoplasmsPrognosisAntineoplastic AgentsProtein IsoformsProtein Kinase InhibitorsProto-Oncogene Proteins c-aktRNA, Small InterferingAkt inhibitorsAkt isoformsovarian cancertumor development

Identifiers

PMID27533079
PMCPMC5342704
OpenAlexW2515930796

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.