Evidence map›Paper›PMID 32686661›Full record

ArticleCell death & disease2020

Inactivating p53 is essential for nerve growth factor receptor to promote melanoma-initiating cell-stemmed tumorigenesis.

Leiwei Jiang, Shibo Huang, Jieqiong Wang, Yiwei Zhang, Yuqing Xiong, Shelya X Zeng, Hua Lu

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

17 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
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  7. The tumor-nerve circuit in breast cancer.Cancer metastasis reviews · 2023
    Review
  8. Article
  9. Article
  10. p53 Family in Resistance to Targeted Therapy of Melanoma.International journal of molecular sciences · 2022
    Review
  11. Review
  12. Review
  13. Inactivation of the tumor suppressor p53 by long noncoding RNA RMRP.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  14. Review
  15. The p75FEBS open bio · 2021
    Article
  16. Article
  17. 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

7 authors at 2 institutions in 2 countries.

Leiwei Jiang *Department of Biochemistry and Molecular Biology, Tulane University School of Medicine, New Orleans, LA, 70112, USA.
Shibo Huang *Department of Biochemistry and Molecular Biology, Tulane University School of Medicine, New Orleans, LA, 70112, USA.
Jieqiong WangDepartment of Biochemistry and Molecular Biology, Tulane University School of Medicine, New Orleans, LA, 70112, USA.
Yiwei ZhangDepartment of Biochemistry and Molecular Biology, Tulane University School of Medicine, New Orleans, LA, 70112, USA.
Yuqing XiongClinical Pharmacology Institute, Nanchang University, Nanchang, Jiangxi, 330006, China.
Shelya X ZengDepartment of Biochemistry and Molecular Biology, Tulane University School of Medicine, New Orleans, LA, 70112, USA.
Hua LuDepartment of Biochemistry and Molecular Biology, Tulane University School of Medicine, New Orleans, LA, 70112, USA. hlu2@tulane.edu.
Tulane University · USNanchang University · CN

Funding

The Role of Ribosomal Proteins in the P53-MDM2 PathwayR01CA095441 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI LU, HUA · 2002 to 2021
$5.1M
Role of the AMPK-MDMX-p53 pathway in cancerR01CA127724 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI LU, HUA · 2007 to 2019
$3.0M
Digital Nanoplasmonic Quantification of Tumor-derived Extracellular Vesicles in Plasma MicrosamplesU01CA252965 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI HU, TONY Y., LU, HUA · 2020 to 2024
$3.0M
Dual Targeting of the p53 pathway for development of anti-cancer therapyR01CA172468 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI LU, HUA · 2012 to 2016
$1.5M
NCI NIH HHS R01 CA095441NCI NIH HHS R01 CA127724NCI NIH HHS R01 CA172468NCI NIH HHS U01 CA252965
6 · The paper itself

Abstract

Nerve growth factor receptor (NGFR, CD271, or p75NTR) is highly expressed in melanoma-initiating cells (MICs) and is critical for their proliferation and tumorigenesis, and yet the underlying mechanism(s) remain incompletely understood. We previously showed that NGFR inhibits p53 activity in a negative feedback manner in various cancer cells. Here we report that this feedback inhibition of p53 by NGFR plays an essential role in maintaining the sphere formation (stem-like phenotype) and proliferation of MICs, and in promoting MIC-derived melanoma growth in vivo. Knockdown of NGFR markedly reduced the size and number of spheroid formation of melanoma cells, which can be rescued by ectopically expressed NGFR. This reduction was also reversed by depleting p53. Consistently, knockdown of NGFR led to the suppression of MIC-derived xenograft tumor growth by inducing the p53 pathway. These results demonstrate that the NGFR-p53 feedback loop is essential for maintaining MIC stem-like phenotype and MIC-derived tumorigenesis, and further validates NGFR as a potential target for developing a molecule-based therapy against melanoma.

Indexed as

Aldehyde DehydrogenaseAnimalsCarcinogenesisCell Line, TumorCell ProliferationClone CellsGene SilencingHumansMelanomaMice, NudeNeoplastic Stem CellsReceptor, Nerve Growth FactorSignal TransductionSpheroids, CellularTumor Stem Cell AssayTumor Suppressor Protein p53Aldehyde DehydrogenaseReceptor, Nerve Growth FactorTumor Suppressor Protein p53

Identifiers

PMID32686661
PMCPMC7371866
OpenAlexW3043673741

What OpenQuestion holds

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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.