Evidence map›Paper›PMID 27807478›Full record

ArticleCell discovery2016

A novel mutant p53 binding partner BAG5 stabilizes mutant p53 and promotes mutant p53 GOFs in tumorigenesis.

Xuetian Yue, Yuhan Zhao, Grace Huang, Jun Li, Junlan Zhu, Zhaohui Feng, Wenwei Hu

Open access · goldAbstract read
In one paragraph

Article in Cell discovery, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.3field-weighted citation impact, top 17% 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

20 citing papers in PubMed, 31 citations in OpenAlex.

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  12. Cancer Stemness: p53 at the Wheel.Frontiers in oncology · 2020
    Review
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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 1 country.

Xuetian YueDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers the State University of New Jersey , New Brunswick, NJ, USA.
Yuhan ZhaoDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers the State University of New Jersey , New Brunswick, NJ, USA.
Grace HuangDepartment of Environmental Medicine, Nelson Institute of Environmental Medicine, New York University School of Medicine , Tuxedo, NY, USA.
Jun LiDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers the State University of New Jersey , New Brunswick, NJ, USA.
Junlan ZhuDepartment of Environmental Medicine, Nelson Institute of Environmental Medicine, New York University School of Medicine , Tuxedo, NY, USA.
Zhaohui FengDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers the State University of New Jersey , New Brunswick, NJ, USA.
Wenwei HuDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers the State University of New Jersey, New Brunswick, NJ, USA; Department of Pharmacology, Rutgers the State University of New Jersey, New Brunswick, NJ, USA.
Rutgers, The State University of New Jersey · USNew York University · US

Funding

The Role of LIF, a Novel Negative Regulator of p53, in Colorectal CancerR01CA160558 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI HU, WENWEI · 2012 to 2017
$1.6M
The role of glutaminase 2, a novel p53 target gene in metabolism, in liver cancerR01CA143204 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI FENG, ZHAOHUI · 2010 to 2014
$1.6M
A Mass Spectrometry System for Quantitative ProteomicsS10OD016400 · OD · RBHS-ROBERT WOOD JOHNSON MEDICAL SCHOOL · PI LOBEL, PETER · 2014 to 2014
$561k
NCI NIH HHS R01 CA143204NCI NIH HHS R01 CA160558NIH HHS S10 OD016400
6 · The paper itself

Abstract

Tumor suppressor p53 is the most frequently mutated gene in human tumors. Many tumor-associated mutant p53 (mutp53) proteins gain new tumor-promoting activities, including increased proliferation, metastasis and chemoresistance of tumor cells, which are defined as gain-of-functions (GOFs). Mutp53 proteins often accumulate at high levels in human tumors, which is important for mutp53 to exert their GOFs. The mechanism underlying mutp53 proteins accumulation in tumors is not fully understood. Here, we report that BAG5, a member of Bcl-2-associated athanogene (BAG) family proteins, promotes mutp53 accumulation in tumors, which in turn enhances mutp53 GOFs. Mechanistically, BAG5 interacts with mutp53 proteins to protect mutp53 from ubiquitination and degradation by E3 ubiquitin ligases MDM2 and CHIP, which in turn promotes mutp53 protein accumulation and therefore GOFs in promoting cell proliferation, tumor growth, cell migration and chemoresistance. BAG5 is frequently overexpressed in many human tumors and the overexpression of BAG5 is associated with poor prognosis of cancer patients. Altogether, this study revealed that inhibition of mutp53 degradation by BAG5 is a novel and critical mechanism underlying mutp53 protein accumulation and GOFs in cancer. Furthermore, our results also uncovered that promoting mutp53 accumulation and GOFs is a novel mechanism of BAG5 in tumorigenesis.

Indexed as

BAG5metastasismutant p53 GOFsubiquitination

Identifiers

PMID27807478
PMCPMC5088412
OpenAlexW2547140447

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.