Evidence map›Paper›PMID 33924987›Full record

ArticleCells2021

The ECM Modulator ITIH5 Affects Cell Adhesion, Motility and Chemotherapeutic Response of Basal/Squamous-Like (BASQ) Bladder Cancer Cells.

Michael Rose, Erik Noetzel, Jennifer Kistermann, Julian Eschenbruch, Sandra Rushrush, Lin Gan, Ruth Knüchel, Nadine T Gaisa, Edgar Dahl

Open access · goldAbstract read
In one paragraph

Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
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  8. Review
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  11. Characterization of the Limbal Epithelial Stem Cell Niche.Investigative ophthalmology & visual science · 2023
    Article
  12. Article
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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

9 authors at 2 institutions in 1 country.

Michael RoseInstitute of Pathology, University Hospital RWTH Aachen University, 52074 Aachen, Germany.ORCID 0000-0002-4340-1117
Erik NoetzelInstitute of Biological Information Processing 2 (IBI-2), Mechanobiology, Forschungszentrum Jülich GmbH, 52425 Jülich, Germany.ORCID 0000-0003-3163-6848
Jennifer KistermannInstitute of Pathology, University Hospital RWTH Aachen University, 52074 Aachen, Germany.ORCID 0000-0002-5845-7973
Julian EschenbruchInstitute of Biological Information Processing 2 (IBI-2), Mechanobiology, Forschungszentrum Jülich GmbH, 52425 Jülich, Germany.ORCID 0000-0002-3430-3590
Sandra RushrushInstitute of Pathology, University Hospital RWTH Aachen University, 52074 Aachen, Germany.
Lin GanIZKF Aachen, Medical Faculty, RWTH Aachen University, 52074 Aachen, Germany.
Ruth KnüchelInstitute of Pathology, University Hospital RWTH Aachen University, 52074 Aachen, Germany.
Nadine T GaisaInstitute of Pathology, University Hospital RWTH Aachen University, 52074 Aachen, Germany.ORCID 0000-0002-4762-3964
Edgar DahlInstitute of Pathology, University Hospital RWTH Aachen University, 52074 Aachen, Germany.ORCID 0000-0002-8439-7994
RWTH Aachen University · DEForschungszentrum Jülich · DE

Funding

Medical Faculty of the RWTH Aachen University (START program). 113/15
6 · The paper itself

Abstract

This study aims at characterizing the role of the putative tumor suppressor ITIH5 in basal-type bladder cancers (BLCA). By sub-classifying TCGA BLCA data, we revealed predominant loss of ITIH5 expression in the basal/squamous-like (BASQ) subtype. ITIH5 expression inversely correlated with basal-type makers such as KRT6A and CD44. Interestingly, Kaplan-Meier analyses showed longer recurrence-free survival in combination with strong CD44 expression, which is thought to mediate ITIH-hyaluronan (HA) binding functions. In vitro, stable ITIH5 overexpression in two basal-type BLCA cell lines showing differential CD44 expression levels, i.e., with (SCaBER) and without squamous features (HT1376), demonstrated clear inhibition of cell and colony growth of BASQ-type SCaBER cells. ITIH5 further enhanced HA-associated cell-matrix attachment, indicated by altered size and number of focal adhesion sites resulting in reduced cell migration capacities. Transcriptomic analyses revealed enrichment of pathways and processes involved in ECM organization, differentiation and cell signaling. Finally, we provide evidence that ITIH5 increase sensitivity of SCaBER cells to chemotherapeutical agents (cisplatin and gemcitabine), whereas responsiveness of HT1376 cells was not affected by ITIH5 expression. Thus, we gain further insights into the putative role of ITIH5 as tumor suppressor highlighting an impact on drug response potentially via the HA-CD44 axis in BASQ-type BLCA.

Indexed as

Gene Expression Regulation, NeoplasticAntineoplastic Combined Chemotherapy ProtocolsApoptosisBiomarkers, TumorCarcinoma, Squamous CellCell AdhesionCell ProliferationCisplatinDeoxycytidineDNA MethylationGemcitabineHumansNeoplasms, Basal CellPrognosisPromoter Regions, GeneticProteinase Inhibitory Proteins, SecretoryBiomarkers, TumorCisplatinDeoxycytidineGemcitabineITIH5 protein, humanProteinase Inhibitory Proteins, SecretoryBASQ subtypebladder cancerCD44chemosensitizerhyaluronanITIH5

Identifiers

PMID33924987
PMCPMC8146567
OpenAlexW3158683121

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.