Evidence map›Paper›PMID 30131448›Full record

ArticleMolecular cancer research : MCR2019

p53-Pirh2 Complex Promotes Twist1 Degradation and Inhibits EMT.

Yang Yang-Hartwich, Roslyn Tedja, Cai M Roberts, Jamie Goodner-Bingham, Carlos Cardenas, Marta Gurea, Natalia J Sumi, Ayesha B Alvero, Carlotta A Glackin, Gil Mor

Abstract read
In one paragraph

Article in Molecular cancer research : MCR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
–field-weighted citation impact
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

34 citing papers in PubMed.

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  11. MAPKs in the early steps of senescence implemEMTation.Frontiers in cell and developmental biology · 2023
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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

10 authors.

Yang Yang-Hartwich *Department of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, New Haven, Connecticut.
Roslyn Tedja *Department of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, New Haven, Connecticut.
Cai M RobertsDepartment of Stem Cell and Developmental Biology, City of Hope Beckman Research Institute, Duarte, California.
Jamie Goodner-BinghamDepartment of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, New Haven, Connecticut.
Carlos CardenasDepartment of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, New Haven, Connecticut.
Marta GureaDepartment of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, New Haven, Connecticut.
Natalia J SumiDepartment of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, New Haven, Connecticut.
Ayesha B AlveroDepartment of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, New Haven, Connecticut.
Carlotta A GlackinDepartment of Stem Cell and Developmental Biology, City of Hope Beckman Research Institute, Duarte, California.
Gil MorDepartment of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, New Haven, Connecticut. gil.mor@yale.edu.

Funding

Targeting the vascularity for delivery of inhibitors of metastasis in ovarian cancer.R01CA199004 · NCI · YALE UNIVERSITY · PI LIU, HAIPENG, MOR, GIL G · 2015 to 2019
$2.5M
NCI NIH HHS R01 CA199004
6 · The paper itself

Abstract

Epithelial-mesenchymal transition (EMT) is a critical process involved in cancer metastasis and chemoresistance. Twist1 is a key EMT-inducing transcription factor, which is upregulated in multiple types of cancers and has been shown to promote tumor cell invasiveness and support tumor progression. Conversely, p53 is a tumor suppressor gene that is frequently mutated in cancers. This study demonstrates the ability of wild-type (WT) p53 to promote the degradation of Twist1 protein. By forming a complex with Twist1 and the E3 ligase Pirh2, WT p53 promotes the ubiquitination and proteasomal degradation of Twist1, thus inhibiting EMT and maintaining the epithelial phenotype. The ability of p53 to induce Twist1 degradation is abrogated when p53 is mutated. Consequently, the loss of p53-induced Twist1 degradation leads to EMT and the acquisition of a more invasive cancer phenotype.

Indexed as

Cell Line, TumorCystadenocarcinoma, SerousEpithelial-Mesenchymal TransitionFemaleHEK293 CellsHumansMutationNuclear ProteinsOvarian NeoplasmsProteasome Endopeptidase ComplexTumor Suppressor Protein p53Twist-Related Protein 1Ubiquitin-Protein LigasesNuclear ProteinsProteasome Endopeptidase ComplexRCHY1 protein, humanTP53 protein, humanTumor Suppressor Protein p53TWIST1 protein, humanTwist-Related Protein 1Ubiquitin-Protein Ligases

Identifiers

PMID30131448
PMCPMC6800184

What OpenQuestion holds

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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.