Evidence map›Paper›PMID 31546993›Full record

ArticleCells2019

HtrA4 Protease Promotes Chemotherapeutic-Dependent Cancer Cell Death.

Tomasz Wenta, Michal Rychlowski, Miroslaw Jarzab, Barbara Lipinska

Open access · goldAbstract read
In one paragraph

Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
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  8. 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

4 authors at 2 institutions in 1 country.

Tomasz WentaDepartment of General and Medical Biochemistry, Faculty of Biology, University of Gdansk, Wita Stwosza 59, 80-308 Gdansk, Poland. tomasz.wenta@biol.ug.edu.pl.
Michal RychlowskiLaboratory of Virus Molecular Biology, Intercollegiate Faculty of Biotechnology, University of Gdansk and Medical University of Gdansk, Abrahama 58, 80-307 Gdansk, Poland. michal.rychlowski@biotech.ug.edu.pl.
Miroslaw JarzabDepartment of General and Medical Biochemistry, Faculty of Biology, University of Gdansk, Wita Stwosza 59, 80-308 Gdansk, Poland. miroslaw.jarzab@biol.ug.edu.pl.
Barbara LipinskaDepartment of General and Medical Biochemistry, Faculty of Biology, University of Gdansk, Wita Stwosza 59, 80-308 Gdansk, Poland. barbara.lipinska@biol.ug.edu.pl.
University of Gdańsk · PLGdańsk Medical University · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The HtrA4 human protease is crucial in placentation and embryo implantation, and its altered level is connected with pre-eclampsia. The meta-analyses of microarray assays revealed that the HtrA4 level is changed in brain tumors and breast and prostate cancers, which suggests its involvement in oncogenesis. In spite of the HtrA4 involvement in important physiological and pathological processes, its function in the cell is poorly understood. In this work, using lung and breast cancer cell lines, we showed for the first time that the full-length HtrA4 and its N-terminally deleted variant promote cancer cell death induced by chemotherapeutic drugs by enhancing apoptosis. The effect is dependent on the HtrA4 proteolytic activity, and the N-terminally deleted HtrA4 is more efficient in the cell death stimulation. Furthermore, HtrA4 increases the effect of chemotherapeutics on the clonogenic potential and motility of cancer cells, and it increases cell cycle arrest at the G2/M phase. HtrA4 may modulate cell death by degrading the anti-apoptotic XIAP protein and also by proteolysis of the executioner pro-caspase 7 and cytoskeletal proteins, actin and β-tubulin. These findings provide new insight into the mechanism of the HtrA4 protease function in cell death and oncogenesis, and they may help to develop new anti-cancer therapeutic strategies.

Indexed as

A549 CellsAntineoplastic AgentsApoptosisCell DeathCells, CulturedCell Transformation, NeoplasticDrug Resistance, NeoplasmHumansMCF-7 CellsMitochondriaNeoplasmsPC-3 CellsSecretory PathwaySerine ProteasesAntineoplastic AgentsHtrA4 protein, humanSerine ProteasesapoptosiscancerHtrA4 proteaseHtrA proteinsoncogenesis

Identifiers

PMID31546993
PMCPMC6829446
OpenAlexW2974826910

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.