Evidence map›Paper›PMID 34503205›Full record

ArticleCancers2021

Kallikrein 5 Inhibition by the Lympho-Epithelial Kazal-Type Related Inhibitor Hinders Matriptase-Dependent Carcinogenesis.

Elaine Zayas Marcelino da Silva, Thais Fernanda de Campos Fraga-Silva, Yao Yuan, Márcia Gaião Alves, Gabriel Azevedo Publio, Carol Kobori da Fonseca, Márcio Hideki Kodama, Gabriel Viliod Vieira, Marina Ferreira Candido, Lara Maria Alencar Ramos Innocentini and 6 more

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

Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.5field-weighted citation impact, top 39% 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

8 citing papers in PubMed, 8 citations in OpenAlex.

  1. MMP1 and PRSS23 induce PARCommunications biology · 2026
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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

16 authors at 2 institutions in 2 countries.

Elaine Zayas Marcelino da SilvaDepartment of Cell and Molecular Biology and Pathogenic Bioagents, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto 14049-900, SP, Brazil.ORCID 0000-0002-2749-6275
Thais Fernanda de Campos Fraga-SilvaBasic and Applied Immunology Program, Department of Biochemistry and Immunology, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto 14049-900, SP, Brazil.ORCID 0000-0002-2053-8938
Yao YuanLaboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Márcia Gaião AlvesDepartment of Cell and Molecular Biology and Pathogenic Bioagents, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto 14049-900, SP, Brazil.
Gabriel Azevedo PublioDepartament of Pharmacology, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto 14049-900, SP, Brazil.ORCID 0000-0002-5643-409X
Carol Kobori da FonsecaDepartment of Cell and Molecular Biology and Pathogenic Bioagents, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto 14049-900, SP, Brazil.ORCID 0000-0002-3072-7142
Márcio Hideki KodamaDepartment of Cell and Molecular Biology and Pathogenic Bioagents, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto 14049-900, SP, Brazil.
Gabriel Viliod VieiraDepartment of Cell and Molecular Biology and Pathogenic Bioagents, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto 14049-900, SP, Brazil.
Marina Ferreira CandidoDepartment of Cell and Molecular Biology and Pathogenic Bioagents, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto 14049-900, SP, Brazil.ORCID 0000-0003-0389-5287
Lara Maria Alencar Ramos InnocentiniDentistry and Stomatology Division, Ophthalmology, Otolaryngology, and Head and Neck Surgery Department, Clinical Hospital of Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto 14049-900, SP, Brazil.
Mateus Gonçalves MirandaDepartment of Cell and Molecular Biology and Pathogenic Bioagents, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto 14049-900, SP, Brazil.
Alfredo Ribeiro da SilvaDepartment of Pathology and Legal Medicine, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto 14049-900, SP, Brazil.
Jose Carlos Alves-FilhoDepartament of Pharmacology, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto 14049-900, SP, Brazil.ORCID 0000-0002-9918-8714
Vania Luiza Deperon BonatoBasic and Applied Immunology Program, Department of Biochemistry and Immunology, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto 14049-900, SP, Brazil.ORCID 0000-0003-4189-2685
Ramiro Iglesias-BartolomeLaboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0002-0792-1254
Katiuchia Uzzun SalesDepartment of Cell and Molecular Biology and Pathogenic Bioagents, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto 14049-900, SP, Brazil.
Universidade de São Paulo · BRNational Institutes of Health · US

Funding

Fundação de Amparo à Pesquisa do Estado de São Paulo 2014/06316-2Fundação de Apoio ao Ensino, Pesquisa e Assistência do Hospital das Clínicas da Faculdade de Medicina de Ribeirão Preto da Universidade de São Paulo NA
6 · The paper itself

Abstract

Head and neck squamous cell carcinoma remains challenging to treat with no improvement in survival rates over the past 50 years. Thus, there is an urgent need to discover more reliable therapeutic targets and biomarkers for HNSCC. Matriptase, a type-II transmembrane serine protease, induces malignant transformation in epithelial stem cells through proteolytic activation of pro-HGF and PAR-2, triggering PI3K-AKT-mTOR and NFKB signaling. The serine protease inhibitor lympho-epithelial Kazal-type-related inhibitor (LEKTI) inhibits the matriptase-driven proteolytic pathway, directly blocking kallikreins in epithelial differentiation. Hence, we hypothesized LEKTI could inhibit matriptase-dependent squamous cell carcinogenesis, thus implicating kallikreins in this process. Double-transgenic mice with simultaneous expression of matriptase and LEKTI under the keratin-5 promoter showed a prominent rescue of K5-Matriptase

Indexed as

KLK5LEKTImatriptaseOSCCSPINK5

Identifiers

PMID34503205
PMCPMC8431081
OpenAlexW3197005456

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.