Evidence map›Paper›PMID 36690946›Full record

ReviewCellular & molecular biology letters2023

TRIM8: a double-edged sword in glioblastoma with the power to heal or hurt.

Hamed Hosseinalizadeh, Omid Mohamadzadeh, Mohammad Saeed Kahrizi, Zahra Razaghi Bahabadi, Daniel J Klionsky, Hamed Mirzei

Open access · goldAbstract readReviewLetter
In one paragraph

Review in Cellular & molecular biology letters, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

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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

6 authors at 5 institutions in 2 countries.

Hamed HosseinalizadehDepartment of Medical Biotechnology, Faculty of Paramedicine, Guilan University of Medical Sciences, Rasht, Iran.
Omid MohamadzadehDepartment of Neurosurgery, Tehran University of Medical Science, Tehran, Iran.
Mohammad Saeed KahriziDepartment of Surgery, Alborz University of Medical Sciences, Karaj, Alborz, Iran.
Zahra Razaghi BahabadiSchool of Medicine, Kashan University of Medical Sciences, Kashan, Iran.
Daniel J KlionskyLife Sciences Institute and Department of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI, USA.
Hamed MirzeiResearch Center for Biochemistry and Nutrition in Metabolic Diseases, Institute for Basic Sciences, Kashan University of Medical Sciences, Kashan, Iran. mirzaei-h@kaums.ac.ir.
Kashan University of Medical Sciences · IRAlborz University of Medical SciencesGuilan University of Medical Sciences · IRUniversity of Michigan–Ann Arbor · USUniversity of Tehran · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) is an aggressive primary brain tumor and one of the most lethal central nervous system tumors in adults. Despite significant breakthroughs in standard treatment, only about 5% of patients survive 5 years or longer. Therefore, much effort has been put into the search for identifying new glioma-associated genes. Tripartite motif-containing (TRIM) family proteins are essential regulators of carcinogenesis. TRIM8, a member of the TRIM superfamily, is abnormally expressed in high-grade gliomas and is associated with poor clinical prognosis in patients with glioma. Recent research has shown that TRIM8 is a molecule of duality (MoD) that can function as both an oncogene and a tumor suppressor gene, making it a "double-edged sword" in glioblastoma development. This characteristic is due to its role in selectively regulating three major cellular signaling pathways: the TP53/p53-mediated tumor suppression pathway, NFKB/NF-κB, and the JAK-STAT pathway essential for stem cell property support in glioma stem cells. In this review, TRIM8 is analyzed in detail in the context of GBM and its involvement in essential signaling and stem cell-related pathways. We also discuss the basic biological activities of TRIM8 in macroautophagy/autophagy, regulation of bipolar spindle formation and chromosomal stability, and regulation of chemoresistance, and as a trigger of inflammation.

Indexed as

GlioblastomaGliomaCarrier ProteinsHumansJanus KinasesNerve Tissue ProteinsNF-kappa BSignal TransductionSTAT Transcription FactorsCarrier ProteinsJanus KinasesNerve Tissue ProteinsNF-kappa BSTAT Transcription FactorsTRIM8 protein, humanAutophagyGlioblastomaJAK-STATNF-κBp53Stem-cellTRIM8

Identifiers

PMID36690946
PMCPMC9869596
OpenAlexW4317734480

What OpenQuestion holds

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Registered trials

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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.