Evidence map›Paper›PMID 28808307›Full record

ArticleScientific reports2017

LC3A Silencing Hinders Aggresome Vimentin Cage Clearance in Primary Choroid Plexus Carcinoma.

Marwa Nassar, Heba Samaha, Myret Ghabriel, Maha Yehia, Hala Taha, Sherin Salem, Khaled Shaaban, Mariam Omar, Nabil Ahmed, Shahenda El-Naggar

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 20% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 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

10 authors at 1 institution in 2 countries.

Marwa NassarTumor Biology Research Program, Basic Research Unit, Department of Research, Children's Cancer Hospital Egypt 57357, P.O Box 11441, 1 Seket Al-Emam Street, Cairo, Egypt.
Heba SamahaTumor Biology Research Program, Basic Research Unit, Department of Research, Children's Cancer Hospital Egypt 57357, P.O Box 11441, 1 Seket Al-Emam Street, Cairo, Egypt.
Myret GhabrielTumor Biology Research Program, Basic Research Unit, Department of Research, Children's Cancer Hospital Egypt 57357, P.O Box 11441, 1 Seket Al-Emam Street, Cairo, Egypt.
Maha YehiaDepartment of Pathology, Children's Cancer Hospital Egypt 57357, P.O Box 11441, 1 Seket Al-Emam Street, Cairo, Egypt.
Hala TahaDepartment of Pathology, Children's Cancer Hospital Egypt 57357, P.O Box 11441, 1 Seket Al-Emam Street, Cairo, Egypt.
Sherin SalemDepartment of Clinical Pathology, Children's Cancer Hospital Egypt 57357, P.O Box 11441, 1 Seket Al-Emam Street, Cairo, Egypt.
Khaled ShaabanDepartment of Clinical Pathology, Children's Cancer Hospital Egypt 57357, P.O Box 11441, 1 Seket Al-Emam Street, Cairo, Egypt.
Mariam OmarTumor Biology Research Program, Basic Research Unit, Department of Research, Children's Cancer Hospital Egypt 57357, P.O Box 11441, 1 Seket Al-Emam Street, Cairo, Egypt.
Nabil AhmedTumor Biology Research Program, Basic Research Unit, Department of Research, Children's Cancer Hospital Egypt 57357, P.O Box 11441, 1 Seket Al-Emam Street, Cairo, Egypt.
Shahenda El-NaggarTumor Biology Research Program, Basic Research Unit, Department of Research, Children's Cancer Hospital Egypt 57357, P.O Box 11441, 1 Seket Al-Emam Street, Cairo, Egypt. shahenda.elnaggar@57357.org.
Children Cancer Hospital · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aggresomes are transient microtubule-dependent inclusion bodies that sequester misfolded proteins and are ultimately removed by autophagy. Here we report the generation of a choroid plexus carcinoma cell line; Children's Cancer Hospital Egypt (CCHE)-45, which is characterized by the constitutive formation of aggresomes. When examining the autophagy pathway as the main route for aggresomes clearance, CCHE-45 cells displayed increased autophagy flux mediated by MAP1LC3B. MAP1LC3A-Variant1 gene expression was silenced by promoter methylation. Restoring MAP1LC3A-Variant1 expression resulted in the formation of MAP1LC3A positive autophagosmes and the disruption of the aggresomes' vimentin cage independent of MAP1LC3B positive autophagosomes. Our data supports the notion that basal quality control autophagy and vimentin cage clearance in CCHE-45 are mediated by MAP1LC3A. Hence we propose that absence of MAP1LC3A disrupts the autophagic pathway and leads to the failure of aggresome vimentin cage degradation. Consequently, this could represent a targetable pathway in autophagy-dependent cancers.

Indexed as

AutophagyAdolescentAutophagosomesCarcinomaCell Line, TumorCells, CulturedChildChoroid Plexus NeoplasmsFemaleGene SilencingHEK293 CellsHumansMaleMicrotubule-Associated ProteinsVimentinMAP1LC3A protein, humanMicrotubule-Associated ProteinsVimentin

Identifiers

PMID28808307
PMCPMC5556083
OpenAlexW2745261779

What OpenQuestion 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 OpenQuestion graph.