Evidence map›Paper›PMID 42794556›Full record

ArticleInternational journal of molecular sciences2026

Combined Modulation of Ceramide and S1P Pathways Induces Strong Cytotoxicity in SH-SY5Y Neuroblastoma Cells.

Celal Ozbek Cakir, Canan Vejselova Sezer, Mustafa Cengiz, Hatice Mehtap Kutlu

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

4 authors.

Celal Ozbek CakirDepartment of Neurosurgery, Afyon Park Hayat Hospital, Afyon 03100, Türkiye.ORCID 0000-0002-3618-6033
Canan Vejselova SezerDepartment of Biology, Kutahya Dumlupinar University, Kütahya 43000, Türkiye.
Mustafa CengizDepartment of Mathematics and Physical Sciences Education, Siirt University, Siirt 56100, Türkiye.ORCID 0000-0002-6925-8371
Hatice Mehtap KutluDepartment of Biology, Eskisehir Technical University, Eskisehir 26470, Türkiye.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuroblastoma is among the most aggressive pediatric cancers, and resistance to standard therapies highlights the need for alternative strategies targeting lipid metabolism and apoptosis-associated pathways. This study aimed to investigate the cytotoxic and apoptotic effects of fingolimod, ceranib-2, and carmofur, administered individually and in combination, in SH-SY5Y neuroblastoma cells, with particular emphasis on ceramide metabolism. Cytotoxicity was evaluated using the MTT assay, and morphological alterations were assessed by confocal microscopy. Colony-forming ability was examined using a soft agar assay, apoptosis-associated responses were evaluated by Annexin-V staining and caspase 3/7 activation analysis, and intracellular ceramide levels were determined using an ELISA-based method. The results showed that all three compounds reduced cell viability in a concentration-dependent manner and decreased clonogenic survival. The triple combination produced the most pronounced changes in apoptosis-associated parameters and showed marked inhibition of colony formation, although fingolimod alone exhibited the lowest IC

Indexed as

CeramidesLysophospholipidsNeuroblastomaSphingosineApoptosisCell Line, TumorCell SurvivalFingolimod HydrochlorideHumansMorpholinesSignal TransductionCeramidesFingolimod HydrochlorideLysophospholipidsMorpholinesRV 538Sphingosinesphingosine 1-phosphateapoptosiscarmofurceramideceranib-2fingolimodneuroblastoma

Identifiers

PMID42794556
PMCPMC13607863

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.