Evidence map›Paper›PMID 32285119›Full record

ArticleJournal of molecular cell biology2020

Inhibition of tumor suppressor p73 by nerve growth factor receptor via chaperone-mediated autophagy.

Daniel Nguyen, Kun Yang, Lucia Chiao, Yun Deng, Xiang Zhou, Zhen Zhang, Shelya X Zeng, Hua Lu

Open access · goldAbstract read
In one paragraph

Article in Journal of molecular cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.8field-weighted citation impact, top 25% 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

15 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
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  10. Radiotherapy modulates tumor cell fate decisions: a review.Radiation oncology (London, England) · 2022
    Review
  11. Article
  12. Review
  13. Mechanisms of Functional Pleiotropy of p73 in Cancer and Beyond.Frontiers in cell and developmental biology · 2021
    Review
  14. Review
  15. 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

8 authors at 2 institutions in 2 countries.

Daniel NguyenDepartment of Biochemistry and Molecular Biology, Tulane Cancer Center, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Kun YangDepartment of Biochemistry and Molecular Biology, Tulane Cancer Center, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Lucia ChiaoDepartment of Biochemistry and Molecular Biology, Tulane Cancer Center, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Yun DengDepartment of Biochemistry and Molecular Biology, Tulane Cancer Center, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Xiang ZhouDepartment of Biochemistry and Molecular Biology, Tulane Cancer Center, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Zhen ZhangDepartment of Radiation Oncology, Shanghai Cancer Center, Department of Oncology, Shanghai Medical School, Fudan University, Shanghai 200032, China.
Shelya X ZengDepartment of Biochemistry and Molecular Biology, Tulane Cancer Center, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Hua LuDepartment of Biochemistry and Molecular Biology, Tulane Cancer Center, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Tulane University · USFudan University Shanghai Cancer Center · 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
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 CA172468
6 · The paper itself

Abstract

The tumor suppressr p73 is a homolog of p53 and is capable of inducing cell cycle arrest and apoptosis. Here, we identify nerve growth factor receptor (NGFR, p75NTR, or CD271) as a novel negative p73 regulator. p73 activates NGFR transcription, which, in turn, promotes p73 degradation in a negative feedback loop. NGFR directly binds to p73 central DNA-binding domain and suppresses p73 transcriptional activity as well as p73-mediated apoptosis in cancer cells. Surprisingly, we uncover a previously unknown mechanism of NGFR-facilitated p73 degradation through the chaperone-mediated autophagy (CMA) pathway. Collectively, our studies demonstrate a new oncogenic function for NGFR in inactivating p73 activity by promoting its degradation through the CMA.

Indexed as

Chaperone-Mediated AutophagyCell Line, TumorCell ProliferationDown-RegulationGene Expression Regulation, NeoplasticHumansProtein BindingProteolysisProto-Oncogene Proteins c-mdm2Receptor, Nerve Growth FactorTranscriptional ActivationTranscription FactorsTumor Protein p73Tumor Suppressor ProteinsProto-Oncogene Proteins c-mdm2Receptor, Nerve Growth FactorTP63 protein, humanTranscription FactorsTumor Protein p73Tumor Suppressor Proteinschaperone-mediated autophagyHSPA8Lamp2aNGFRp73

Identifiers

PMID32285119
PMCPMC7749740
OpenAlexW3015534970

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.