Evidence map›Paper›PMID 41129070›Full record

ArticleStem cell reviews and reports2026

Nestin and SOX2 Maintain self-renewal Abilities of Different Pancreatic Cancer Stem Cell Populations.

Lisa-Marie Philipp, Patrick Hoffmann, Luisa Hattingen, Amelie Modi, Susanne Sebens

Abstract read
In one paragraph

Article in Stem cell reviews and reports, 2026. 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

5 authors.

Lisa-Marie PhilippInstitute for Experimental Cancer Research, Kiel University and University Hospital Schleswig-Holstein Campus Kiel, Kiel, Germany.
Patrick HoffmannInstitute for Experimental Cancer Research, Kiel University and University Hospital Schleswig-Holstein Campus Kiel, Kiel, Germany.
Luisa HattingenInstitute for Experimental Cancer Research, Kiel University and University Hospital Schleswig-Holstein Campus Kiel, Kiel, Germany.
Amelie ModiInstitute for Experimental Cancer Research, Kiel University and University Hospital Schleswig-Holstein Campus Kiel, Kiel, Germany.
Susanne SebensInstitute for Experimental Cancer Research, Kiel University and University Hospital Schleswig-Holstein Campus Kiel, Kiel, Germany. susanne.sebens@email.uni-kiel.de.ORCID 0000-0001-6582-0083

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metastasis and therapy resistance are main clinical challenges of pancreatic ductal adenocarcinoma (PDAC) still limiting patient`s prognosis. Both are dependent on tumor cell plasticity, which allows rapid adaptation of tumor cells to changing microenvironmental conditions. Epithelial-Mesenchymal-Transition (EMT), a process by which carcinoma cells acquire invasive abilities, is associated with a gain of cancer stem cell (CSC) properties. Different CSC phenotypes were described in PDAC, whereby high levels of the CSC marker Nestin was identified in CSC clones of mesenchymal Panc1 cells, while CSC clones of epithelial Panc89 cells were characterized by a high SOX2 expression. To investigate the functional impact of these CSC markers in PDAC cells with different EMT phenotypes, expression of either CSC marker was silenced in heterogenous (parental) and CSC PDAC populations to analyze their impact on essential malignancy associated properties.SiRNA-mediated knockdown (KD) of NES and/or SOX2 in Panc1 and Panc89 cell variants (parental and CSC population), respectively, was successfully achieved. Decreased NES expression in Panc1 cell variants and decreased SOX2 expression in Panc89 cell variants significantly inhibited self-renewing properties, however, only marginally impacted cell growth, EMT marker expression, migration and invasion properties as well as response to chemotherapy. Overall, our data indicate that Nestin and SOX2 are crucial mediators of self-renewal capabilities of mesenchymal and epithelial PDAC cell variants, respectively, but that further factors are required for the maintenance of other malignancy associated properties.

Indexed as

Carcinoma, Pancreatic DuctalCell Self RenewalNeoplastic Stem CellsNestinPancreatic NeoplasmsSOXB1 Transcription FactorsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansNES protein, humanNestinSOX2 protein, humanSOXB1 Transcription FactorsCancer stem cellsChemoresistanceEpithelial-to-Mesenchymal transitionInvasionMetastasisPancreatic ductal adenocarcinomaPlasticity

Identifiers

PMID41129070
PMCPMC12795969

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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.