Evidence map›Paper›PMID 38002001›Full record

ReviewBiomedicines2023

Role of Akt/Protein Kinase B in Cancer Metastasis.

Mohammad Islam, Sarah Jones, Ian Ellis

Open access · goldAbstract readReview
In one paragraph

Review in Biomedicines, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Akt-phosphorylated UFL1 UFMylates ArpC4 to promote metastasis.Nature structural & molecular biology · 2025
    Article
  9. Article
  10. Journal of virology · 2025
    Article
  11. Article
  12. Review
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

3 authors at 1 institution in 1 country.

Mohammad IslamUnit of Cell and Molecular Biology, School of Dentistry, University of Dundee, Park Place, Dundee DD1 4HR, UK.ORCID 0000-0003-0792-4540
Sarah JonesUnit of Cell and Molecular Biology, School of Dentistry, University of Dundee, Park Place, Dundee DD1 4HR, UK.
Ian EllisUnit of Cell and Molecular Biology, School of Dentistry, University of Dundee, Park Place, Dundee DD1 4HR, UK.ORCID 0000-0001-8035-6012
University of Dundee · GB

Funding

Anonymous Trust N/AScottish Overseas Research Student Award Scheme N/A
6 · The paper itself

Abstract

Metastasis is a critical step in the process of carcinogenesis and a vast majority of cancer-related mortalities result from metastatic disease that is resistant to current therapies. Cell migration and invasion are the first steps of the metastasis process, which mainly occurs by two important biological mechanisms, i.e., cytoskeletal remodelling and epithelial to mesenchymal transition (EMT). Akt (also known as protein kinase B) is a central signalling molecule of the PI3K-Akt signalling pathway. Aberrant activation of this pathway has been identified in a wide range of cancers. Several studies have revealed that Akt actively engages with the migratory process in motile cells, including metastatic cancer cells. The downstream signalling mechanism of Akt in cell migration depends upon the tumour type, sites, and intracellular localisation of activated Akt. In this review, we focus on the role of Akt in the regulation of two events that control cell migration and invasion in various cancers including head and neck squamous cell carcinoma (HNSCC) and the status of PI3K-Akt pathway inhibitors in clinical trials in metastatic cancers.

Indexed as

Aktcancercytoskeletal remodellingEMTHNSCCmetastasis

Identifiers

PMID38002001
PMCPMC10669635
OpenAlexW4388538942

What Socratic 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 Socratic graph.