Evidence map›Paper›PMID 31471556›Full record

ArticleProstate cancer and prostatic diseases2020

Therapeutic potential of ReACp53 targeting mutant p53 protein in CRPC.

Yaqun Zhang, Lingfan Xu, Yan Chang, YanJing Li, William Butler, Er Jin, Aifen Wang, Yulei Tao, Xufeng Chen, Chaozhao Liang and 1 more

Open access · greenAbstract read
In one paragraph

Article in Prostate cancer and prostatic diseases, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 12% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Targeting p53 pathways: mechanisms, structures, and advances in therapy.Signal transduction and targeted therapy · 2023
    Pooled it
  2. Review
  3. Review
  4. Targeting mitochondria and programmed cell death as potential interventions for metastatic castration-resistant prostate cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Polygenic anti-cancer activity ofToxicology reports · 2024
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Anticancer Therapeutic Strategies Targeting p53 Aggregation.International journal of molecular sciences · 2022
    Review
  20. Review
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

11 authors at 5 institutions in 2 countries.

Yaqun Zhang *Department of Urology, Beijing Hospital, National Center of Gerontology, Beijing, China.
Lingfan Xu *Department of Pathology, Duke University Medicine, Durham, NC, USA.
Yan ChangDepartment of Pathology, Duke University Medicine, Durham, NC, USA.
YanJing LiDepartment of Pathology, Duke University Medicine, Durham, NC, USA.
William ButlerDepartment of Pathology, Duke University Medicine, Durham, NC, USA.
Er JinDepartment of Pathology, Duke University Medicine, Durham, NC, USA.
Aifen WangDepartment of Pathology, Duke University Medicine, Durham, NC, USA.
Yulei TaoDepartment of Pathology, Duke University Medicine, Durham, NC, USA.
Xufeng ChenDepartment of Pathology, Duke University Medicine, Durham, NC, USA.
Chaozhao LiangDepartment of Urology, the First Affiliated Hospital of Anhui Medical University, Hefei, China. liang_chaozhao@163.com.
Jiaoti HuangDepartment of Pathology, Duke University Medicine, Durham, NC, USA. jiaoti.huang@duke.edu.
Duke University · USAnhui Medical University · CNBeijing Hospital · CNFirst Affiliated Hospital of Anhui Medical University · CNHangzhou First People's Hospital · CN

Funding

Systems Analysis of Epigenomic Architecture in Cancer ProgressionU54CA217297 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI HUANG, TIM H.-M. · 2017 to 2021
$9.3M
Identification of DNA methylation markers for risk of metastasis in localized proR01CA181242 · NCI · KAISER FOUNDATION RESEARCH INSTITUTE · PI CHAO, CHUN R. · 2015 to 2019
$3.0M
Role and targeting of PRMT5 in prostate cancerR01CA212403 · NCI · PURDUE UNIVERSITY · PI HUANG, JIAOTI, LI, CHENGLONG · 2017 to 2021
$3.0M
Role of oncogenic phosphorylated MED1 in aggressive prostate cancerR01CA200853 · NCI · OHIO STATE UNIVERSITY · PI CLINTON, STEVEN K, HUANG, JIAOTI · 2017 to 2021
$1.9M
A novel strategy to identify prostate cancer biomarkers for patient managementR01CA172603 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI HUANG, JIAOTI · 2013 to 2017
$1.6M
Histologic and Immunohistochemical Biomarkers for Heavily Treated Metastatic Prostate Cancer.R01CA205001 · NCI · DUKE UNIVERSITY · PI HUANG, JIAOTI · 2016 to 2020
$1.3M
NCI NIH HHS R01 CA172603NCI NIH HHS R01 CA181242NCI NIH HHS R01 CA200853NCI NIH HHS R01 CA205001NCI NIH HHS R01 CA212403NCI NIH HHS U54 CA217297NIH HHS 1R01CA172603NIH HHS 1R01CA181242
6 · The paper itself

Abstract

backgroundsp53 is a tumor suppressor that prevents cancer onset and progression, and mutations in the p53 gene cause loss of the tumor suppressor function of the protein. The mutant p53 protein in tumor cells can form aggregates which contribute to the dominant-negative effect over the wild-type p53 protein, causing loss of p53 tumor suppression or gain of novel oncogenic functions. Mutations in p53 have been implicated in the pathogenesis of primary prostate cancer (PCa), and are often detected in recurrent and metastatic disease. Thus, targeting mutant p53 may constitute an alternative therapeutic strategy for advanced PCa for which there are no other viable options.

methodsIn this study, we used immunoprecipitation, immunofluorescence, clonogenic survival, and cell proliferation assays, flow cytometric analysis and in vivo xenograft to investigate the biological effects of ReACp53, a cell-permeable peptide inhibitor of p53 aggregation, on mutant p53-carrying PCa cells.

resultsOur results show that ReACp53 targets amyloid aggregates of mutant p53 protein and restores the p53 nuclear function as transcriptional factor, induces mitochondrial cell death and reduces DNA synthesis of mutant p53-carrying PCa cells; ReACp53 also inhibits xenograft tumor growth in vivo.

conclusionsThe data presented here suggest a therapeutic potential of targeting mutant p53 protein in advanced PCa setting, which has a clinical impact for aggressive PCa with transforming how such tumors are managed.

Indexed as

Molecular Targeted TherapyMutationAnimalsAntineoplastic Agents, HormonalApoptosisCell CycleCell Line, TumorCell-Penetrating PeptidesCell ProliferationDisease Models, AnimalDrug Resistance, NeoplasmHumansMaleMembrane Potential, MitochondrialMiceMitochondriaAntineoplastic Agents, HormonalCell-Penetrating PeptidesReceptors, AndrogenTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID31471556
PMCPMC7031025
OpenAlexW2971182584

What OpenQuestion holds

Textmetadata
LicenceTDM
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.