Evidence map›Paper›PMID 25263447›Full record

ArticleOncogene2015

p53 protein aggregation promotes platinum resistance in ovarian cancer.

Y Yang-Hartwich, M G Soteras, Z P Lin, J Holmberg, N Sumi, V Craveiro, M Liang, E Romanoff, J Bingham, F Garofalo and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

77 citing papers in PubMed, 156 citations in OpenAlex.

  1. The p53 Isoforms as Potential Biomarkers in Different Cancer Entities.International journal of molecular sciences · 2026
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  9. Cancer medicine · 2024
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  20. Article

17 more citing papers are in PubMed but not listed here.

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

12 authors at 1 institution in 1 country.

Y Yang-HartwichDepartment of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, CT, USA.
M G SoterasDepartment of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, CT, USA.
Z P LinDepartment of Pharmacology, Yale University School of Medicine, New Haven, CT, USA.
J HolmbergDepartment of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, CT, USA.
N SumiDepartment of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, CT, USA.
V CraveiroDepartment of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, CT, USA.
M LiangDepartment of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, CT, USA.
E RomanoffDepartment of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, CT, USA.
J BinghamDepartment of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, CT, USA.
F GarofaloDepartment of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, CT, USA.
A AlveroDepartment of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, CT, USA.
G MorDepartment of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, CT, USA.
Yale University · US

Funding

Apoptotic regulators in ovarian cancerR01CA118678 · NCI · YALE UNIVERSITY · PI MOR, GIL G · 2007 to 2011
$1.7M
MyD88-bearing tumors in immune-regulation and chemo-resistanceR01CA127913 · NCI · YALE UNIVERSITY · PI MOR, GIL G · 2008 to 2012
$1.7M
NCI NIH HHS R01CA118678NCI NIH HHS R01CA127913
6 · The paper itself

Abstract

High-grade serous ovarian carcinoma (HGSOC), the most lethal gynecological cancer, often leads to chemoresistant diseases. The p53 protein is a key transcriptional factor regulating cellular homeostasis. A majority of HGSOCs have inactive p53 because of genetic mutations. However, genetic mutation is not the only cause of p53 inactivation. The aggregation of p53 protein has been discovered in different types of cancers and may be responsible for impairing the normal transcriptional activation and pro-apoptotic functions of p53. We demonstrated that in a unique population of HGSOC cancer cells with cancer stem cell properties, p53 protein aggregation is associated with p53 inactivation and platinum resistance. When these cancer stem cells differentiated into their chemosensitive progeny, they lost tumor-initiating capacity and p53 aggregates. In addition to the association of p53 aggregation and chemoresistance in HGSOC cells, we further demonstrated that the overexpression of a p53-positive regulator, p14ARF, inhibited MDM2-mediated p53 degradation and led to the imbalance of p53 turnover that promoted the formation of p53 aggregates. With in vitro and in vivo models, we demonstrated that the inhibition of p14ARF could suppress p53 aggregation and sensitize cancer cells to platinum treatment. Moreover, by two-dimensional gel electrophoresis and mass spectrometry we discovered that the aggregated p53 may function uniquely by interacting with proteins that are critical for cancer cell survival and tumor progression. Our findings help us understand the poor chemoresponse of a subset of HGSOC patients and suggest p53 aggregation as a new marker for chemoresistance. Our findings also suggest that inhibiting p53 aggregation can reactivate p53 pro-apoptotic function. Therefore, p53 aggregation is a potential therapeutic target for reversing chemoresistance. This is paramount for improving ovarian cancer patients' responses to chemotherapy, and thus increasing their survival rate.

Indexed as

Drug Resistance, NeoplasmAnimalsAntineoplastic AgentsCarboplatinFemaleHumansMiceMice, NudeMutationOvarian NeoplasmsPlatinum CompoundsProtein AggregatesProtein Aggregation, PathologicalTumor Cells, CulturedTumor Suppressor Protein p53Antineoplastic AgentsCarboplatinPlatinum CompoundsProtein AggregatesTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID25263447
OpenAlexW2165851018

What OpenQuestion holds

Textmetadata
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.