ArticleCNS neuroscience & therapeutics2024
SESN1 functions as a new tumor suppressor gene via Toll-like receptor signaling pathway in neuroblastoma.
Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Sestrins: a new therapeutic target for endothelial dysfunction and cardiovascular disease prevention.Annals of medicine · 2025Review
- Immunosenescence-Related Gene MAFF is Involved in Immune Regulation and Malignant Progression in Pancreatic Adenocarcinoma.Biological procedures online · 2025Article
- cfDNA hydroxymethylcytosine profiling for detection metastasis and recurrence of Esophageal Squamous Cell Carcinoma.World journal of surgical oncology · 2025Article
- Molecular regulation and therapeutic targeting ofFrontiers in cell and developmental biology · 2025Review
- SESN1 functions as a new tumor suppressor gene via Toll-like receptor signaling pathway in neuroblastoma.CNS neuroscience & therapeutics · 2024Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
aimsNeuroblastoma (NB) is the most common extracranial solid tumor in children, with a 5-year survival rate of <50% in high-risk patients. MYCN amplification is an important factor that influences the survival rate of high-risk patients. Our results indicated MYCN regulates the expression of SESN1. Therefore, this study aimed to investigate the role and mechanisms of SESN1 in NB.
methodssiRNAs or overexpression plasmids were used to change MYCN, SESN1, or MyD88's expression. The role of SESN1 in NB cell proliferation, migration, and invasion was elucidated. Xenograft mice models were built to evaluate SESN1's effect in vivo. The correlation between SESN1 expression and clinicopathological data of patients with NB was analyzed. RNA-Seq was done to explore SESN1's downstream targets.
resultsSESN1 was regulated by MYCN in NB cells. Knockdown SESN1 promoted NB cell proliferation, cell migration, and cell invasion, and overexpressing SESN1 had opposite functions. Knockdown SESN1 promoted tumor growth and shortened tumor-bearing mice survival time. Low expression of SESN1 had a positive correlation with poor prognosis in patients with NB. RNA-Seq showed that Toll-like receptor (TLR) signaling pathway, and PD-L1 expression and PD-1 checkpoint pathway in cancer were potential downstream targets of SESN1. Knockdown MyD88 or TLRs inhibitor HCQ reversed the effect of knockdown SESN1 in NB cells. High expression of SESN1 was significantly associated with a higher immune score and indicated an active immune microenvironment for patients with NB.
conclusionsSESN1 functions as a new tumor suppressor gene via TLR signaling pathway in NB.
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Registered trials
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 Socratic graph.