Evidence map›Paper›PMID 40753921›Full record

ArticleTranslational oncology2025

KLK5 and KLK7 drive cervical carcinoma via KLK14-dependent RhoA and NF-κB pathways.

Gabriel Viliod Vieira, Rodrigo Alberto Alves da Silva, Letícia Andrade Costa, João Paulo Bianchi Ximenez, Margarita Lamprou, Mateus Gonçalves Miranda, Vitor de Moura Arrais, Bruna Miyoko Ikenaga de Brito, Elaine Zayas Marcelino da Silva, Bruno Belmonte Martinelli Gomes and 13 more

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Article in Translational oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

23 authors.

Gabriel Viliod VieiraDepartment of Cell and Molecular Biology and Pathogenic Bioagents, Ribeirao Preto Medical School, University of Sao Paulo, Sao Paulo, Brazil.
Rodrigo Alberto Alves da SilvaDepartment of Cell and Molecular Biology and Pathogenic Bioagents, Ribeirao Preto Medical School, University of Sao Paulo, Sao Paulo, Brazil.
Letícia Andrade CostaDepartment of Medical Imaging, Hematology, and Clinical Oncology, Ribeirao Preto Medical School, University of Sao Paulo, São Paulo, Brazil.
João Paulo Bianchi XimenezDepartment of Clinical Analyses, Toxicology and Food Science, School of Pharmaceutical Sciences of Ribeirao Preto, University of São Paulo, Sao Paulo, Brazil.
Margarita LamprouDepartment of Pharmacy, University of Patras, Patras, Greece.
Mateus Gonçalves MirandaDepartment of Cell and Molecular Biology and Pathogenic Bioagents, Ribeirao Preto Medical School, University of Sao Paulo, Sao Paulo, Brazil.
Vitor de Moura ArraisDepartment of Cell and Molecular Biology and Pathogenic Bioagents, Ribeirao Preto Medical School, University of Sao Paulo, Sao Paulo, Brazil.
Bruna Miyoko Ikenaga de BritoDepartment of Cell and Molecular Biology and Pathogenic Bioagents, Ribeirao Preto Medical School, University of Sao Paulo, Sao Paulo, Brazil.
Elaine Zayas Marcelino da SilvaDepartment of Cell and Molecular Biology and Pathogenic Bioagents, Ribeirao Preto Medical School, University of Sao Paulo, Sao Paulo, Brazil.
Bruno Belmonte Martinelli GomesDepartment of Cell and Molecular Biology and Pathogenic Bioagents, Ribeirao Preto Medical School, University of Sao Paulo, Sao Paulo, Brazil.
Carol Kobori da FonsecaDepartment of Cell and Molecular Biology and Pathogenic Bioagents, Ribeirao Preto Medical School, University of Sao Paulo, Sao Paulo, Brazil.
Márcia Gaião AlvesDepartment of Cell and Molecular Biology and Pathogenic Bioagents, Ribeirao Preto Medical School, University of Sao Paulo, Sao Paulo, Brazil.
Camila Aparecida Coelho BrazãoDepartment of Cell and Molecular Biology and Pathogenic Bioagents, Ribeirao Preto Medical School, University of Sao Paulo, Sao Paulo, Brazil.
Kevin Luiz Lopes-DelphinoDepartment of Cell and Molecular Biology and Pathogenic Bioagents, Ribeirao Preto Medical School, University of Sao Paulo, Sao Paulo, Brazil.
Laura Miguel RodríguezDepartment of Cell and Molecular Biology and Pathogenic Bioagents, Ribeirao Preto Medical School, University of Sao Paulo, Sao Paulo, Brazil.
Thiago Mattar CunhaDepartment of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Sao Paulo, Brazil.
Ana Paula LepiqueDepartment of Immunology, Biomedical Sciences Institute, University of Sao Paulo, Sao Paulo, Brazil.
Constantinos M MikelisDepartment of Pharmacy, University of Patras, Patras, Greece.
Raphael Sanches PeresDepartment of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Sao Paulo, Brazil.
Wilson Araújo SilvaDepartment of Genetics, Ribeirao Preto Medical School, University of Sao Paulo, Sao Paulo, Brazil.
Leandro Machado ColliDepartment of Medical Imaging, Hematology, and Clinical Oncology, Ribeirao Preto Medical School, University of Sao Paulo, São Paulo, Brazil.
Silvana Maria QuintanaDepartment of Gynecology and Obstetrics, Ribeirao Preto Medical School, University of Sao Paulo, Sao Paulo, Brazil.
Katiuchia Uzzun SalesDepartment of Cell and Molecular Biology and Pathogenic Bioagents, Ribeirao Preto Medical School, University of Sao Paulo, Sao Paulo, Brazil. Electronic address: salesk@fmrp.usp.br.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe global prevalence of Human Papillomavirus (HPV) infection is approximately 12%, which significantly contributes to the development of cervical cancer as HPV is a key driver of tumorigenesis. However, the precise mechanisms by which HPV promotes carcinogenesis and the involvement of additional components in this process remain poorly understood.

objectiveGiven the evidence supporting the critical role of serine proteases in carcinogenesis, we investigated their contribution to cervical cancer development in the context of HPV-mediated carcinogenesis.

methodsHuman biopsies were analyzed to assess the expression of serine proteases, including matriptase, kallikrein 5 (KLK5), and kallikrein 7 (KLK7), as well as their endogenous inhibitors. Mechanistic studies were conducted using genetically engineered mice, bulk RNA-seq, and reporter assays to elucidate the role of these proteases in HPV-dependent cervical carcinogenesis.

resultsOur findings demonstrate increased expression of matriptase, KLK5, and KLK7 in early cervical carcinogenesis. Furthermore, the absence of both KLK5 and KLK7 ameliorates the HPV-dependent phenotype via modulation of KLK14 activation. KLK14 exhibits a pro-tumorigenic effect by regulating PAR-2-dependent RhoA and NF-κB signaling pathways.

conclusionThis study underscores the critical roles of serine proteases KLK5, KLK7, and KLK14 in cervical carcinogenesis, suggesting that these serine proteases are promising targets for the development of novel therapeutic strategies in cervical cancer.

Indexed as

Cervical carcinomaHigh-grade squamous intraepithelial lesionKallikrein 14Kallikrein 5Kallikrein 7RhoA and NFkBSerine proteases

Identifiers

PMID40753921
PMCPMC12375203

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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.