Evidence map›Paper›PMID 32071790›Full record

ArticleJournal of advanced research2020

Overexpression of alpha-synuclein promotes both cell proliferation and cell toxicity in human SH-SY5Y neuroblastoma cells.

Noela Rodríguez-Losada, Javier de la Rosa, María Larriva, Rune Wendelbo, José A Aguirre, Javier S Castresana, Santiago J Ballaz

Open access · goldAbstract read
In one paragraph

Article in Journal of advanced research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.2field-weighted citation impact, top 10% 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

27 citing papers in PubMed, 40 citations in OpenAlex.

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  8. A hypothesis explaining Alzheimer's disease, Parkinson's disease, and dementia with Lewy bodies overlap.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
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  18. Genetic Elements at the Alpha-Synuclein Locus.Frontiers in neuroscience · 2022
    Review
  19. Article
  20. 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

7 authors at 4 institutions in 3 countries.

Noela Rodríguez-LosadaDept. of Human Physiology & Physical Sports Education, Medical School, University of Málaga, Málaga, Spain.
Javier de la RosaDept. of Biochemistry & Genetics, University of Navarra School of Sciences, Pamplona, Spain.
María LarrivaDept. of Pharmacology & Toxicology, University of Navarra School of Pharmacy and Nutrition, Pamplona, Spain.
Rune WendelboAbalonyx AS, Oslo, Norway.
José A AguirreDept. of Human Physiology & Physical Sports Education, Medical School, University of Málaga, Málaga, Spain.
Javier S CastresanaDept. of Biochemistry & Genetics, University of Navarra School of Sciences, Pamplona, Spain.
Santiago J BallazSchool of Biological Sciences & Engineering, Yachay Tech University, Urcuquí, Ecuador.
Universidad de Navarra · ESUniversidad de Málaga · ESAbalonyx (Norway) · NOUniversidad Yachay Tech · EC

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alpha-Synuclein (aSyn) is a chameleon-like protein. Its overexpression and intracellular deposition defines neurodegenerative α-synucleinopathies including Parkinson's disease. Whether aSyn up-regulation is the cause or the protective reaction to α-synucleinopathies remains unresolved. Remarkably, the accumulation of aSyn is involved in cancer. Here, the neuroblastoma SH-SY5Y cell line was genetically engineered to overexpress aSyn at low and at high levels. aSyn cytotoxicity was assessed by the MTT and vital-dye exclusion methods, observed at the beginning of the sub-culture of low-aSyn overexpressing neurons when cells can barely proliferate exponentially. Conversely, high-aSyn overexpressing cultures grew at high rates while showing enhanced colony formation compared to low-aSyn neurons. Cytotoxicity of aSyn overexpression was indirectly revealed by the addition of pro-oxidant rotenone. Pretreatment with partially reduced graphene oxide, an apoptotic agent, increased toxicity of rotenone in low-aSyn neurons, but, it did not in high-aSyn neurons. Consistent with their enhanced proliferation, high-aSyn neurons showed elevated levels of SMP30, a senescence-marker protein, and the mitosis Ki-67 marker. High-aSyn overexpression conferred to the carcinogenic neurons heightened tumorigenicity and resistance to senescence compared to low-aSyn cells, thus pointing to an inadequate level of aSyn stimulation, rather than the aSyn overload itself, as one of the factors contributing to α-synucleinopathy.

Indexed as

Alpha-synucleinCell senescenceGraphene oxideParkinson’s diseaseRotenoneSH-SY5Y cells

Identifiers

PMID32071790
PMCPMC7016025
OpenAlexW3002262768

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.