Evidence map›Paper›PMID 38413795›Full record

ArticleOncogene2024

AF1q is a universal marker of neuroblastoma that sustains N-Myc expression and drives tumorigenesis.

Babak Oskouian, Joanna Y Lee, Shahab Asgharzadeh, Ranjha Khan, Meng Zhang, Julia R Weisbrod, Youn-Jeong Choi, Latika Puri, Ana E Aguilar, Piming Zhao and 1 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncogene, 2024. 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
1.1field-weighted citation impact, top 24% of its field
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, 3 citations in OpenAlex.

  1. Review
  2. Molecular regulation and therapeutic targeting ofFrontiers in cell and developmental biology · 2025
    Review
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

11 authors at 4 institutions in 1 country.

Babak OskouianDepartment of Pediatrics and the Helen Diller Family Comprehensive Cancer Center, University of California at San Francisco, San Francisco, CA, USA.
Joanna Y LeeDepartment of Pediatrics and the Helen Diller Family Comprehensive Cancer Center, University of California at San Francisco, San Francisco, CA, USA.
Shahab AsgharzadehChildren's Hospital of Los Angeles, University of Southern California, Los Angeles, CA, USA.
Ranjha KhanDepartment of Pediatrics and the Helen Diller Family Comprehensive Cancer Center, University of California at San Francisco, San Francisco, CA, USA.
Meng ZhangDepartment of Pediatrics and the Helen Diller Family Comprehensive Cancer Center, University of California at San Francisco, San Francisco, CA, USA.
Julia R WeisbrodDepartment of Pediatrics and the Helen Diller Family Comprehensive Cancer Center, University of California at San Francisco, San Francisco, CA, USA.
Youn-Jeong ChoiDepartment of Pediatrics and the Helen Diller Family Comprehensive Cancer Center, University of California at San Francisco, San Francisco, CA, USA.
Latika PuriLoma Linda University Children's Hospital, Loma Linda, CA, USA.
Ana E AguilarArnold Palmer Hospital for Children, Orlando, FL, USA.
Piming ZhaoDepartment of Pediatrics and the Helen Diller Family Comprehensive Cancer Center, University of California at San Francisco, San Francisco, CA, USA.
Julie D SabaDepartment of Pediatrics and the Helen Diller Family Comprehensive Cancer Center, University of California at San Francisco, San Francisco, CA, USA. Julie.Saba@ucsf.edu.ORCID 0000-0002-4894-919X
UCSF Helen Diller Family Comprehensive Cancer Center · USArnold Palmer Hospital for Children · USLoma Linda University Children's Hospital · USUniversity of Southern California · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuroblastoma is the most common extracranial malignant tumor of childhood, accounting for 15% of all pediatric cancer deaths. Despite significant advances in our understanding of neuroblastoma biology, five-year survival rates for high-risk disease remain less than 50%, highlighting the importance of identifying novel therapeutic targets to combat the disease. MYCN amplification is the most frequent and predictive molecular aberration correlating with poor outcome in neuroblastoma. N-Myc is a short-lived protein primarily due to its rapid proteasomal degradation, a potentially exploitable vulnerability in neuroblastoma. AF1q is an oncoprotein with established roles in leukemia and solid tumor progression. It is normally expressed in brain and sympathetic neurons and has been postulated to play a part in neural differentiation. However, no role for AF1q in tumors of neural origin has been reported. In this study, we found AF1q to be a universal marker of neuroblastoma tumors. Silencing AF1q in neuroblastoma cells caused proteasomal degradation of N-Myc through Ras/ERK and AKT/GSK3β pathways, activated p53 and blocked cell cycle progression, culminating in cell death via the intrinsic apoptotic pathway. Moreover, silencing AF1q attenuated neuroblastoma tumorigenicity in vivo signifying AF1q's importance in neuroblastoma oncogenesis. Our findings reveal AF1q to be a novel regulator of N-Myc and potential therapeutic target in neuroblastoma.

Indexed as

NeuroblastomaCarcinogenesisCell Line, TumorCell Transformation, NeoplasticChildGene Expression Regulation, NeoplasticHumansN-Myc Proto-Oncogene ProteinOncogene ProteinsTranscription FactorsN-Myc Proto-Oncogene ProteinOncogene ProteinsTranscription Factors

Identifiers

PMID38413795
PMCPMC11014797
OpenAlexW4392188197

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.