ArticleCell death discovery2026
MYCN inhibits TrkC-mediated differentiation in neuroblastoma cells via disruption of the PKA signalling pathway.
Article in Cell death discovery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- Review
- A temporal (phospho-)proteomic dataset of neurotrophic receptor tyrosine kinase signalling in neuroblastoma.Scientific data · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Neuroblastoma is a rare childhood cancer in which high-risk disease, frequently driven by MYCN amplification, has poor survival. Trk-receptor expression correlates with prognosis: TrkA is observed in low-risk cases while TrkB is often expressed in high-risk MYCN-amplified neuroblastoma. However, TrkC's role in neuroblastoma genesis remains unclear. This study investigates the interplay between TrkC signalling and MYCN status. Using neuroblastoma cell lines with varying MYCN levels, we found that TrkC activation leads to neuronal differentiation in MYCN non-amplified cells but promotes proliferation in MYCN-overexpressing and MYCN-amplified cells. Temporal phosphoproteomic analysis identified the PKA pathway as crucial for TrkC-mediated differentiation. Manipulating PKA signalling altered cell fate in vitro and in zebrafish xenografts. In MYCN-amplified cells, MYCN knockdown enhanced PKA/CREB signalling and induced differentiation. Similarly, overexpression of constitutively active PKA or CREB promoted differentiation, confirming the role of PKA/CREB pathway in driving differentiation. Analysis of patient data revealed reduced expression of PKA pathway genes in MYCN-amplified tumours. Additionally, MYCN-induced miR-221 was found to suppress CREB expression. Together, these findings demonstrate MYCN-dependent effects of TrkC signalling and highlight the therapeutic potential of targeting the PKA pathway to induce differentiation in high-risk MYCN-amplified neuroblastoma.
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.