Evidence map›Paper›PMID 40445424›Full record

ArticleMedical oncology (Northwood, London, England)2025

Investigating the antiproliferative mechanisms of NaHS, a hydrogen sulfide donor, in the SH-SY5Y cell line.

Ayşegül Öztürk, Ziad Joha, Neslihan Başgöz, Ahmet Şevki Taşkıran

Abstract read
In one paragraph

Article in Medical oncology (Northwood, London, England), 2025. 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
–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

2 citing papers in PubMed.

  1. Article
  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

4 authors.

Ayşegül ÖztürkDepartments of Therapy and Rehabilitation, Vocational School of Health Services, Sivas Cumhuriyet University, Sivas, Türkiye. aysegulozturk@cumhuriyet.edu.tr.
Ziad JohaDepartments of Pharmacology, Faculty of Pharmacy, Sivas Cumhuriyet University, Sivas, Turkey.
Neslihan BaşgözDepartment of Physiology, Medicine Faculty, Sivas Cumhuriyet University, Sivas, Türkiye.
Ahmet Şevki TaşkıranDepartment of Physiology, Medicine Faculty, Sivas Cumhuriyet University, Sivas, Türkiye.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuroblastoma, a childhood cancer, arises from neural crest cells within the sympathetic nervous system. This study investigated the anticancer effects of the exogenous hydrogen sulfide (H₂S) donor, sodium hydrogen sulfide (NaHS), on neuroblastoma cells, elucidating how it inhibits cell proliferation. The study was conducted using the SH-SY5Y cell line. The cells were exposed to various concentrations of NaHS (32, 16, 8, 4, and 2 mM) for 24 h. Cell viability was assessed using the XTT assay. ELISA was used to measure levels of the growth signal factors HER-2, EGFR, mTOR, ERK-1, and ERK-2, as well as the apoptosis marker caspase-3. In addition, apoptosis was evaluated using the Muse Annexin V & Dead Cell Assay Kit. NaHS significantly reduced cell proliferation, as demonstrated by the XTT assay (p < 0.001). NaHS treatment also decreased levels of HER-2, EGFR, ERK-1, and ERK-2 (p < 0.05 to p < 0.01), while mTOR levels remained unchanged (p > 0.05) and caspase-3 levels increased (p < 0.001). Flow cytometry confirmed that NaHS treatment significantly increased the proportion of apoptotic cells (p < 0.001). The antiproliferative effect of NaHS against neuroblastoma appears to be mediated through the suppression of certain growth signal factors and the induction of apoptosis. These findings suggest that exogenous hydrogen sulfide donors hold promise as a potential therapeutic strategy for neuroblastoma.

Indexed as

Cell ProliferationHydrogen SulfideNeuroblastomaSulfidesApoptosisCell Line, TumorCell SurvivalHumansHydrogen Sulfidesodium bisulfideSulfidesApoptosisEGFRHydrogen sulfideNaHSSH-SY5Y

Identifiers

PMID40445424
PMCPMC12125090

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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.