Evidence map›Paper›PMID 36834476›Full record

ReviewInternational journal of molecular sciences2023

Ran GTPase and Its Importance in Cellular Signaling and Malignant Phenotype.

Mohamed El-Tanani, Hamdi Nsairat, Vijay Mishra, Yachana Mishra, Alaa A A Aljabali, Ángel Serrano-Aroca, Murtaza M Tambuwala

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
9.5field-weighted citation impact, top 1% 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

31 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
  2. Article
  3. SpatialESD: Spatial Ensemble Domain Detection in Spatial Transcriptomics.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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  19. Review
  20. Impact ofBiomolecules & biomedicine · 2024
    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

7 authors at 5 institutions in 4 countries.

Mohamed El-TananiPharmacological and Diagnostic Research Centre, Faculty of Pharmacy, Al-Ahliyya Amman University, Amman 19328, Jordan.ORCID 0000-0002-4735-5445
Hamdi NsairatPharmacological and Diagnostic Research Centre, Faculty of Pharmacy, Al-Ahliyya Amman University, Amman 19328, Jordan.ORCID 0000-0001-5916-5879
Vijay MishraSchool of Pharmaceutical Sciences, Lovely Professional University, Phagwara 144411, India.ORCID 0000-0001-6542-2464
Yachana MishraDepartment of Zoology, School of Bioengineering and Biosciences, Lovely Professional University, Phagwara 144411, India.ORCID 0000-0002-3467-0518
Alaa A A AljabaliDepartment of Pharmaceutics & Pharmaceutical Technology, Yarmouk University, Irbid 21163, Jordan.ORCID 0000-0002-9519-6338
Ángel Serrano-ArocaBiomaterials and Bioengineering Laboratory, Centro de Investigación Traslacional San Alberto Magno, Universidad Católica de Valencia San Vicente Mártir, c/Guillem de Castro 94, 46001 Valencia, Spain.ORCID 0000-0002-9953-3848
Murtaza M TambuwalaLincoln Medical School, University of Lincoln, Brayford Pool, Lincoln LN6 7TS, UK.ORCID 0000-0001-8499-9891
Al-Ahliyya Amman University · JOLovely Professional University · INUniversity of Lincoln · GBValencia Catholic University Saint Vincent Martyr · ESYarmouk University · JO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ran is a member of the Ras superfamily of proteins, which primarily regulates nucleocytoplasmic trafficking and mediates mitosis by regulating spindle formation and nuclear envelope (NE) reassembly. Therefore, Ran is an integral cell fate determinant. It has been demonstrated that aberrant Ran expression in cancer is a result of upstream dysregulation of the expression of various factors, such as osteopontin (OPN), and aberrant activation of various signaling pathways, including the extracellular-regulated kinase/mitogen-activated protein kinase (ERK/MEK) and phosphatidylinositol 3-kinase/Protein kinase B (PI3K/Akt) pathways. In vitro, Ran overexpression has severe effects on the cell phenotype, altering proliferation, adhesion, colony density, and invasion. Therefore, Ran overexpression has been identified in numerous types of cancer and has been shown to correlate with tumor grade and the degree of metastasis present in various cancers. The increased malignancy and invasiveness have been attributed to multiple mechanisms. Increased dependence on Ran for spindle formation and mitosis is a consequence of the upregulation of these pathways and the ensuing overexpression of Ran, which increases cellular dependence on Ran for survival. This increases the sensitivity of cells to changes in Ran concentration, with ablation being associated with aneuploidy, cell cycle arrest, and ultimately, cell death. It has also been demonstrated that Ran dysregulation influences nucleocytoplasmic transport, leading to transcription factor misallocation. Consequently, patients with tumors that overexpress Ran have been shown to have a higher malignancy rate and a shorter survival time compared to their counterparts.

Indexed as

GTP PhosphohydrolasesNeoplasmsHumansPhenotypePhosphatidylinositol 3-Kinasesran GTP-Binding ProteinGTP PhosphohydrolasesPhosphatidylinositol 3-Kinasesran GTP-Binding ProteinaneuploidymetastasismitosisosteopontinRan GTPase

Identifiers

PMID36834476
PMCPMC9968026
OpenAlexW4319318666

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.