Evidence map›Paper›PMID 39446152›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2025

Chaetocin inhibits the progression of neuroblastoma by targeting JAK2/STAT3 signaling pathway in SH-SY5Y cells.

Ke Wang, Ye Li, Linlin Wang

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Article in Naunyn-Schmiedeberg's archives of pharmacology, 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
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1 · What the graph read from it

What it found

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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.

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Ke WangDepartment of Neurosurgery, 3201 Hospital, Hanzhong, 723000, China.
Ye LiDepartment of Oncology, Kunming Children's Hospital, Kunming, 650000, China.
Linlin WangDepartment of Neurosurgery, The Second Affiliated Hospital of Xi'an Medical College, Xi'an, Shaanxi, 710038, PR China. wanglinfmmu@sina.com.ORCID 0000-0003-2161-3490

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chaetocin is a fungal mycotoxin that extensively found in various natural products and has anticancer and anti‑inflammatory activities. Herein, the anticancer effects of chaetocin against the progression of neuroblastoma were studied with SHSY-5Y human neuroblastoma cells and examined the underlying molecular mechanisms. The effects of chaetocin on cellular viability, apoptosis, cell migration, and invasion were investigated. The underlying mechanism of anticancer effects of chaetocin was found to mediate via activating JAK2/STAT3 signaling pathway. Furthermore, when SHSY-5Y cells were exposed to a higher concentration of chaetocin, the induction of cell apoptosis significantly increased by enhancing the expression of pro-apoptotic protein Bcl-2, resulting in anticancer activity against neuroblastoma. In addition, chaetocin significantly decreased the SHSY-5Y cell invasion and migration at 50 μM treatment. Moreover, it was shown that increasing chaetocin treatments greatly decreased the activity of proteins connected to the JAK2/STAT3 signaling pathway. In conclusion, chaetocin exhibits a diverse range of actions on neuroblastoma cells, including the inhibition of proliferation, induction of apoptosis, perturbation of cellular morphology, and modulation of critical signaling pathways, with a specific focus on the JAK/STAT3 pathway. These results contribute valuable insights that underscore the potential therapeutic utility of chaetocin in the context of neuroblastoma treatment, suggesting its multifaceted impact on key cellular processes involved in cancer progression.

Indexed as

Antineoplastic AgentsJanus Kinase 2NeuroblastomaSTAT3 Transcription FactorApoptosisCell Line, TumorCell MovementCell ProliferationCell SurvivalDisease ProgressionHumansPiperazinesSignal TransductionAntineoplastic AgentschaetocinJAK2 protein, humanJanus Kinase 2PiperazinesSTAT3 protein, humanSTAT3 Transcription FactorAnticancer activityApoptosisChaetocinJAK2/STAT3 signaling pathwayNeuroblastoma

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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.