Evidence map›Paper›PMID 38336976›Full record

ReviewCell proliferation2024

The interplay between the PI3K/AKT pathway and circadian clock in physiologic and cancer-related pathologic conditions.

Mohammad Rafi Khezri, Hsiang-Yin Hsueh, Somayeh Mohammadipanah, Javad Khalili Fard, Morteza Ghasemnejad-Berenji

Abstract readReview
In one paragraph

Review in Cell proliferation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
–field-weighted citation impact
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

25 citing papers in PubMed.

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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

5 authors.

Mohammad Rafi KhezriReproductive Health Research Center, Clinical Research Institute, Urmia University of Medical Sciences, Urmia, Iran.ORCID https://orcid.org/0000-0002-4280-0378
Hsiang-Yin HsuehThe Ohio State University Graduate Program in Molecular, Cellular and Developmental Biology, The Ohio State University, Columbus, Ohio, USA.
Somayeh MohammadipanahReproductive Health Research Center, Clinical Research Institute, Urmia University of Medical Sciences, Urmia, Iran.
Javad Khalili FardDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Tabriz University of Medical Sciences, Tabriz, Iran.
Morteza Ghasemnejad-BerenjiDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Urmia University of Medical Sciences, Urmia, Iran.ORCID https://orcid.org/0000-0001-5672-9202

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The circadian clock is responsible for the regulation of different cellular processes, and its disturbance has been linked to the development of different diseases, such as cancer. The main molecular mechanism for this issue has been linked to the crosstalk between core clock regulators and intracellular pathways responsible for cell survival. The PI3K/AKT signalling pathway is one of the most known intracellular pathways in the case of cancer initiation and progression. This pathway regulates different aspects of cell survival including proliferation, apoptosis, metabolism, and response to environmental stimuli. Accumulating evidence indicates that there is a link between the PI3K/AKT pathway activity and circadian rhythm in physiologic and cancer-related pathogenesis. Different classes of PI3Ks and AKT isoforms are involved in regulating circadian clock components in a transcriptional and functional manner. Reversely, core clock components induce a rhythmic fashion in PI3K and AKT activity in physiologic and pathogenic conditions. The aim of this review is to re-examine the interplay between this pathway and circadian clock components in normal condition and cancer pathogenesis, which provides a better understanding of how circadian rhythms may be involved in cancer progression.

Indexed as

Circadian ClocksNeoplasmsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionAnimalsCircadian RhythmHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID38336976
PMCPMC11216939

What OpenQuestion holds

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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.