Evidence map›Paper›PMID 26957636›Full record

ArticleThe Biochemical journal2016

Combinatorial protein engineering of proteolytically resistant mesotrypsin inhibitors as candidates for cancer therapy.

Itay Cohen, Olumide Kayode, Alexandra Hockla, Banumathi Sankaran, Derek C Radisky, Evette S Radisky, Niv Papo

Open access · greenAbstract read
In one paragraph

Article in The Biochemical journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

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  12. Proteases: Pivot Points in Functional Proteomics.Methods in molecular biology (Clifton, N.J.) · 2019
    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 1 institution in 1 country.

Itay CohenDepartment of Biotechnology Engineering and the National Institute of Biotechnology in the Negev, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel.
Olumide KayodeDepartment of Cancer Biology, Mayo Clinic Comprehensive Cancer Center, Jacksonville, FL 32224, U.S.A.
Alexandra HocklaDepartment of Cancer Biology, Mayo Clinic Comprehensive Cancer Center, Jacksonville, FL 32224, U.S.A.
Banumathi SankaranBerkeley Center for Structural Biology, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, U.S.A.
Derek C RadiskyDepartment of Cancer Biology, Mayo Clinic Comprehensive Cancer Center, Jacksonville, FL 32224, U.S.A.
Evette S RadiskyDepartment of Cancer Biology, Mayo Clinic Comprehensive Cancer Center, Jacksonville, FL 32224, U.S.A. radisky.evette@mayo.edu papo@bgu.ac.il.
Niv PapoDepartment of Biotechnology Engineering and the National Institute of Biotechnology in the Negev, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel radisky.evette@mayo.edu papo@bgu.ac.il.
Ben-Gurion University of the Negev · IL

Funding

Inhibiting serine protease-induced prostate cancer progressionR01CA154387 · NCI · MAYO CLINIC JACKSONVILLE · PI RADISKY, EVETTE S · 2013 to 2017
$1.6M
Howard Hughes Medical InstituteNCI NIH HHS R01 CA154387
6 · The paper itself

Abstract

Engineered protein therapeutics offer advantages, including strong target affinity, selectivity and low toxicity, but like natural proteins can be susceptible to proteolytic degradation, thereby limiting their effectiveness. A compelling therapeutic target is mesotrypsin, a protease up-regulated with tumour progression, associated with poor prognosis, and implicated in tumour growth and progression of many cancers. However, with its unique capability for cleavage and inactivation of proteinaceous inhibitors, mesotrypsin presents a formidable challenge to the development of biological inhibitors. We used a powerful yeast display platform for directed evolution, employing a novel multi-modal library screening strategy, to engineer the human amyloid precursor protein Kunitz protease inhibitor domain (APPI) simultaneously for increased proteolytic stability, stronger binding affinity and improved selectivity for mesotrypsin inhibition. We identified a triple mutant APPIM17G/I18F/F34V, with a mesotrypsin inhibition constant (Ki) of 89 pM, as the strongest mesotrypsin inhibitor yet reported; this variant displays 1459-fold improved affinity, up to 350 000-fold greater specificity and 83-fold improved proteolytic stability compared with wild-type APPI. We demonstrated that APPIM17G/I18F/F34V acts as a functional inhibitor in cell-based models of mesotrypsin-dependent prostate cancer cellular invasiveness. Additionally, by solving the crystal structure of the APPIM17G/I18F/F34V-mesotrypsin complex, we obtained new insights into the structural and mechanistic basis for improved binding and proteolytic resistance. Our study identifies a promising mesotrypsin inhibitor as a starting point for development of anticancer protein therapeutics and establishes proof-of-principle for a novel library screening approach that will be widely applicable for simultaneously evolving proteolytic stability in tandem with desired functionality for diverse protein scaffolds.

Indexed as

Amyloid beta-Protein PrecursorAntineoplastic AgentsCell Line, TumorDirected Molecular EvolutionFlow CytometryHumansKineticsMaleNeoplasmsProtease InhibitorsProtein EngineeringSubstrate SpecificityTrypsinAmyloid beta-Protein PrecursorAntineoplastic AgentsProtease InhibitorsPRSS3 protein, humanTrypsincancer therapydirected evolutionenzyme inhibitionmesotrypsinprotease inhibitorprotein engineeringproteolysisX-ray structure

Identifiers

PMID26957636
PMCPMC4898653
OpenAlexW2301971233

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.