Evidence map›Paper›PMID 38167030›Full record

ArticleBMC cancer2024

CLEC19A overexpression inhibits tumor cell proliferation/migration and promotes apoptosis concomitant suppression of PI3K/AKT/NF-κB signaling pathway in glioblastoma multiforme.

Fatemeh Mohajerani, Zahra Moazezi Tehrankhah, Saeid Rahmani, Nastaran Afsordeh, Sajad Shafiee, Mohammad Hossein Pourgholami, Bahram M Soltani, Majid Sadeghizadeh

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

2 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. 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

8 authors at 3 institutions in 1 country.

Fatemeh MohajeraniDepartment of Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Jalal AleAhmad Highway, Tehran, Iran.
Zahra Moazezi TehrankhahDepartment of Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Jalal AleAhmad Highway, Tehran, Iran.
Saeid RahmaniSchool of Computer Science, Institute for Research in Fundamental Sciences (IPM), Tehran, Iran.
Nastaran AfsordehDepartment of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Sajad ShafieeDepartment of Neurosurgery, Mazandaran University of Medical Sciences, Sari, Iran.
Mohammad Hossein PourgholamiDepartment of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Bahram M SoltaniDepartment of Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Jalal AleAhmad Highway, Tehran, Iran.
Majid SadeghizadehDepartment of Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Jalal AleAhmad Highway, Tehran, Iran. sadeghma@modares.ac.ir.
Tarbiat Modares University · IRInstitute for Research in Fundamental Sciences · IRMazandaran University of Medical Sciences · IR

Funding

Iran National Science Foundation 99025431
6 · The paper itself

Abstract

backgroundGBM is the most frequent malignant primary brain tumor in humans. The CLEC19A is a member of the C-type lectin family, which has a high expression in brain tissue. Herein, we sought to carry out an in-depth analysis to pinpoint the role of CLEC19A expression in GBM.

methodsTo determine the localization of CLEC19A, this protein was detected using Western blot, Immunocytochemistry/Immunofluorescence, and confocal microscopy imaging. CLEC19A expression in glioma cells and tissues was evaluated by qRT-PCR. Cell viability, proliferation, migration, and apoptosis were examined through MTT assay, CFSE assay, colony formation, wound healing assay, transwell test, and flow cytometry respectively after CLEC19A overexpression. The effect of CLEC19A overexpression on the PI3K/AKT/NF-κB signaling pathway was investigated using Western blot. An in vivo experiment substantiated the in vitro results using the glioblastoma rat models.

resultsOur in-silico analysis using TCGA data and measuring CLEC19A expression level by qRT-PCR determined significantly lower expression of CLEC19A in human glioma tissues compared to healthy brain tissues. By employment of ICC/IF, confocal microscopy imaging, and Western blot we could show that CLEC19A is plausibly a secreted protein. Results obtained from several in vitro readouts showed that CLEC19A overexpression in U87 and C6 glioma cell lines is associated with the inhibition of cell proliferation, viability, and migration. Further, qRT-PCR and Western blot analysis showed CLEC19A overexpression could reduce the expression levels of PI3K, VEGFα, MMP2, and NF-κB and increase PTEN, TIMP3, RECK, and PDCD4 expression levels in glioma cell lines. Furthermore, flow cytometry results revealed that CLEC19A overexpression was associated with significant cell cycle arrest and promotion of apoptosis in glioma cell lines. Interestingly, using a glioma rat model we could substantiate that CLEC19A overexpression suppresses glioma tumor growth.

conclusionsTo our knowledge, this is the first report providing in-silico, molecular, cellular, and in vivo evidences on the role of CLEC19A as a putative tumor suppressor gene in GBM. These results enhance our understanding of the role of CLEC19A in glioma and warrant further exploration of CLEC19A as a potential therapeutic target for GBM.

Indexed as

GlioblastomaGliomaLectins, C-TypeAnimalsApoptosisApoptosis Regulatory ProteinsCell Line, TumorCell ProliferationGPI-Linked ProteinsHumansNF-kappa BPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRatsRNA-Binding ProteinsSignal TransductionApoptosis Regulatory ProteinsGPI-Linked ProteinsLectins, C-TypeNF-kappa BPDCD4 protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRECK protein, humanRNA-Binding ProteinsCLEC19AC-type lectinGlioblastomaPI3K/AKT/NF-κB pathwayTumor suppressor gene

Identifiers

PMID38167030
PMCPMC10763001
OpenAlexW4390499242

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.