Evidence map›Paper›PMID 31078742›Full record

ReviewPharmacological research2019

The unconventional role of Akt1 in the advanced cancers and in diabetes-promoted carcinogenesis.

Abdulrahman Alwhaibi, Arti Verma, Mir S Adil, Payaningal R Somanath

Open access · greenAbstract readReview
In one paragraph

Review in Pharmacological research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

61 citing papers in PubMed, 93 citations in OpenAlex.

  1. Article
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  5. Targeting the PI3K/AKT/mTOR signaling pathway in prostate cancer: Molecular dysregulation, therapeutic advances, and future directions.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2026
    Review
  6. Therapeutic Potential of Ziyuglycosides fromDrug design, development and therapy · 2026
    Review
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1 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

Abdulrahman AlwhaibiProgram in Clinical and Experimental Therapeutics, College of Pharmacy, University of Georgia and the Charlie Norwood VA Medical Center, Augusta, GA, USA.
Arti VermaProgram in Clinical and Experimental Therapeutics, College of Pharmacy, University of Georgia and the Charlie Norwood VA Medical Center, Augusta, GA, USA.
Mir S AdilProgram in Clinical and Experimental Therapeutics, College of Pharmacy, University of Georgia and the Charlie Norwood VA Medical Center, Augusta, GA, USA.
Payaningal R SomanathProgram in Clinical and Experimental Therapeutics, College of Pharmacy, University of Georgia and the Charlie Norwood VA Medical Center, Augusta, GA, USA; Department of Medicine, Vascular Biology Center and Cancer Center, Augusta University, USA. Electronic address: sshenoy@augusta.edu.
Charlie Norwood VA Medical Center · USAugusta University Health · US

Funding

Implementing a Maternal health and PRegnancy Outcomes Vision for Everyone (IMPROVE)UL1TR002378 · NCATS · EMORY UNIVERSITY · PI Andres J Garcia, Elizabeth O. Ofili · 2017 to 2026
$92.1M
Protein kinase B (Akt)-mediated pathway regulating endothelial-barrier functionR01HL103952 · NHLBI · UNIVERSITY OF GEORGIA · PI SHENOY, SOMANATH P RAMMOHAN · 2011 to 2015
$1.5M
NCATS NIH HHS UL1 TR002378NHLBI NIH HHS R01 HL103952
6 · The paper itself

Abstract

Decades of research have elucidated the critical role of Akt isoforms in cancer as pro-tumorigenic and metastatic regulators through their specific effects on the cancer cells, tumor endothelial cells and the stromal cells. The pro-cancerous role of Akt isoforms through enhanced cell proliferation and suppression of apoptosis in cancer cells and the cells in the tumor microenvironment is considered a dogma. Intriguingly, studies also indicate that the Akt pathway is essential to protect the endothelial-barrier and prevent aberrant vascular permeability, which is also integral to tumor perfusion and metastasis. To complicate this further, a flurry of recent reports strongly indicates the metastasis suppressive role of Akt, Akt1 in particular in various cancer types. These reports emanated from different laboratories have elegantly demonstrated the paradoxical effect of Akt1 on cancer cell epithelial-to-mesenchymal transition, invasion, tumor endothelial-barrier disruption, and cancer metastasis. Here, we emphasize on the specific role of Akt1 in mediating tumor cell-vasculature reciprocity during the advanced stages of cancers and discuss how Akt1 differentially regulates cancer metastasis through mechanisms distinct from its pro-tumorigenic effects. Since Akt is integral for insulin signaling, endothelial function, and metabolic regulation, we also attempt to shed some light on the specific effects of diabetes in modulating Akt pathway in the promotion of tumor growth and metastasis.

Indexed as

AnimalsCapillary PermeabilityCarcinogenesisCell ProliferationDiabetes ComplicationsHumansNeoplasmsNeovascularization, PathologicPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAkt1CancerDiabetesMetastasisTumor endothelium

Identifiers

PMID31078742
PMCPMC6659399
OpenAlexW2944485914

What OpenQuestion holds

Textmetadata
LicenceTDM
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.