Evidence map›Paper›PMID 32604996›Full record

ArticleInternational journal of molecular sciences2020

Quantitative Ultrastructural Morphometry and Gene Expression of mTOR-Related Mitochondriogenesis within Glioblastoma Cells.

Rosangela Ferese, Paola Lenzi, Federica Fulceri, Francesca Biagioni, Cinzia Fabrizi, Stefano Gambardella, Pietro Familiari, Alessandro Frati, Fiona Limanaqi, Francesco Fornai

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

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  10. Alterations of Mitochondrial Structure in Methamphetamine Toxicity.International journal of molecular sciences · 2022
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  16. Review
  17. Review
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 4 institutions in 1 country.

Rosangela FereseI.R.C.C.S. Neuromed, via Atinense 18, 86077 Pozzilli (IS), Italy.
Paola LenziDepartment of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, via Roma 55, 56126 Pisa, Italy.
Federica FulceriDepartment of Clinical and Experimental Medicine University of Pisa, via Roma 55, 56126 Pisa, Italy.
Francesca BiagioniI.R.C.C.S. Neuromed, via Atinense 18, 86077 Pozzilli (IS), Italy.ORCID 0000-0003-3566-4889
Cinzia FabriziDepartment of Anatomy, Histology, Forensic Medicine and Orthopedics, Sapienza University of Rome, Via A. Borelli 50, 00161 Rome, Italy.ORCID 0000-0002-6007-754X
Stefano GambardellaI.R.C.C.S. Neuromed, via Atinense 18, 86077 Pozzilli (IS), Italy.
Pietro FamiliariDepartment of Human Neurosciences, Division of Neurosurgery, Sapienza University of Rome, 00185 Roma, Italy.ORCID 0000-0003-0513-2312
Alessandro FratiI.R.C.C.S. Neuromed, via Atinense 18, 86077 Pozzilli (IS), Italy.
Fiona LimanaqiDepartment of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, via Roma 55, 56126 Pisa, Italy.ORCID 0000-0003-0185-2099
Francesco FornaiI.R.C.C.S. Neuromed, via Atinense 18, 86077 Pozzilli (IS), Italy.ORCID 0000-0002-3883-5084
University of Pisa · ITIstituto Neurologico Mediterraneo · ITSapienza University of Rome · ITUniversity of Urbino · IT

Funding

Ministero della Salute Ricerca Corrente 2020
6 · The paper itself

Abstract

In glioblastoma (GBM) cells, an impairment of mitochondrial activity along with autophagy suppression occurs. Autophagy suppression in GBM promotes stemness, invasion, and poor prognosis. The autophagy deficit seems to be due, at least in part, to an abnormal up-regulation of the mammalian target of rapamycin (mTOR), which may be counteracted by pharmacological mTORC1 inhibition. Since autophagy activation is tightly bound to increased mitochondriogenesis, a defect in the synthesis of novel mitochondria is expected to occur in GBM cells. In an effort to measure a baseline deficit in mitochondria and promote mitochondriogenesis, the present study used two different GBM cell lines, both featuring mTOR hyperactivity. mTORC1 inhibition increases the expression of genes and proteins related to autophagy, mitophagy, and mitochondriogenesis. Autophagy activation was counted by RT-PCR of autophagy genes, LC3- immune-fluorescent puncta and immune-gold, as well as specific mitophagy-dependent BNIP3 stoichiometric increase in situ, within mitochondria. The activation of autophagy-related molecules and organelles after rapamycin exposure occurs concomitantly with progression of autophagosomes towards lysosomes. Remarkably, mitochondrial biogenesis and plasticity (increased mitochondrial number, integrity, and density as well as decreased mitochondrial area) was long- lasting for weeks following rapamycin withdrawal.

Indexed as

Gene Expression Regulation, NeoplasticMitophagyOrganelle BiogenesisGlioblastomaHumansMitochondriaReactive Oxygen SpeciesTOR Serine-Threonine KinasesTumor Cells, CulturedMTOR protein, humanReactive Oxygen SpeciesTOR Serine-Threonine Kinasesautophagylysosomesmitochondrial biogenesismitochondrial constitutive genesmitochondrial DNAmitophagyNRF2PGC1rapamycin

Identifiers

PMID32604996
PMCPMC7370179
OpenAlexW3037633958

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.