Evidence map›Paper›PMID 31711233›Full record

ArticleProtein engineering, design & selection : PEDS2019

Development of a novel prostate apoptosis response-4 (Par-4) protein entity with an extended duration of action for therapeutic treatment of cancer.

Kyungbo Kim, Pereira Araujo, Nikhil Hebbar, Ziyuan Zhou, Xirong Zheng, Fang Zheng, Vivek M Rangnekar, Chang-Guo Zhan

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Protein engineering, design & selection : PEDS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

2 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. 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

8 authors at 2 institutions in 1 country.

Kyungbo KimMolecular Modeling and Biopharmaceutical Center, University of Kentucky, 789 South Limestone Street, Lexington, KY 40356, USA.
Pereira AraujoGraduate Center for Toxicology and Cancer Biology, University of Kentucky, 789 South Limestone Street, Lexington, KY 40356, USA.
Nikhil HebbarGraduate Center for Toxicology and Cancer Biology, University of Kentucky, 789 South Limestone Street, Lexington, KY 40356, USA.
Ziyuan ZhouMolecular Modeling and Biopharmaceutical Center, University of Kentucky, 789 South Limestone Street, Lexington, KY 40356, USA.
Xirong ZhengMolecular Modeling and Biopharmaceutical Center, University of Kentucky, 789 South Limestone Street, Lexington, KY 40356, USA.
Fang ZhengMolecular Modeling and Biopharmaceutical Center, University of Kentucky, 789 South Limestone Street, Lexington, KY 40356, USA.
Vivek M RangnekarGraduate Center for Toxicology and Cancer Biology, University of Kentucky, 789 South Limestone Street, Lexington, KY 40356, USA.
Chang-Guo ZhanMolecular Modeling and Biopharmaceutical Center, University of Kentucky, 789 South Limestone Street, Lexington, KY 40356, USA.
University of Kentucky · USThe Graduate Center, CUNY · US

Funding

Suppression of Prostate Tumor Growth and Metastasis by Inhibition of VimentinR01CA187273 · NCI · UNIVERSITY OF KENTUCKY · PI RANGNEKAR, VIVEK M · 2015 to 2019
$1.7M
NCI NIH HHS R01 CA187273
6 · The paper itself

Abstract

Prostate apoptosis response-4 (Par-4) is a tumor suppressor which protects against neoplastic transformation. Remarkably, Par-4 is capable of inducing apoptosis selectively in cancer cells without affecting the normal cells. In this study, we found that recombinant Par-4 protein had limited serum persistence in mice that may diminish its anti-tumor activity in vivo. To improve the in vivo performance of the short-lived Par-4 protein, we aimed to develop a novel, long-lasting form of Par-4 with extended sequence, denoted as Par-4Ex, without affecting the desirable molecular function of the natural Par-4. We demonstrate that the Par-4Ex protein entity, produced by using the Escherichia coli expression system suitable for large-scale production, fully retains the desirable pro-apoptotic activity of Par-4 protein, but with ~7-fold improved biological half-life. Further in vivo tests confirmed that, due to the prolonged biological half-life, the Par-4Ex protein is indeed more potent in suppressing metastatic tumor growth in mice.

Indexed as

Protein EngineeringAnimalsApoptosisApoptosis Regulatory ProteinsBreast NeoplasmsCell Line, TumorCell ProliferationFemaleHumansLung NeoplasmsMiceTissue DistributionApoptosis Regulatory Proteinsprostate apoptosis response-4 proteinbiological half-lifemetastatic cancerPar-4protein engineeringtherapeutic protein

Identifiers

PMID31711233
PMCPMC7191865
OpenAlexW2985479130

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.