Evidence map›Paper›PMID 33986188›Full record

ArticleJCI insight2021

CD109-GP130 interaction drives glioblastoma stem cell plasticity and chemoresistance through STAT3 activity.

Pauliina Filppu, Jayendrakishore Tanjore Ramanathan, Kirsi J Granberg, Erika Gucciardo, Hannu Haapasalo, Kaisa Lehti, Matti Nykter, Vadim Le Joncour, Pirjo Laakkonen

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

38 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
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  4. Review
  5. Antagonist nanobodies prevent protease inhibition by CD109.The Journal of biological chemistry · 2026
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  13. Rapid cleavage of 6-[EJNMMI radiopharmacy and chemistry · 2025
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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 3 countries.

Pauliina FilppuTranslational Cancer Medicine Research Program, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Jayendrakishore Tanjore RamanathanTranslational Cancer Medicine Research Program, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Kirsi J GranbergFaculty of Medicine and Health Technology, Tampere University, Tampere, Finland.
Erika GucciardoIndividualized Drug Therapy Program, Research Programs Unit, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Hannu HaapasaloDepartment of Pathology, Fimlab Laboratories, Tampere University Hospital and University of Tampere, Tampere, Finland.
Kaisa LehtiIndividualized Drug Therapy Program, Research Programs Unit, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Matti NykterFaculty of Medicine and Health Technology, Tampere University, Tampere, Finland.
Vadim Le JoncourTranslational Cancer Medicine Research Program, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Pirjo LaakkonenTranslational Cancer Medicine Research Program, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
University of Helsinki · FITampere University · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioma stem cells (GSCs) drive propagation and therapeutic resistance of glioblastomas, the most aggressive diffuse brain tumors. However, the molecular mechanisms that maintain the stemness and promote therapy resistance remain poorly understood. Here we report CD109/STAT3 axis as crucial for the maintenance of stemness and tumorigenicity of GSCs and as a mediator of chemoresistance. Mechanistically, CD109 physically interacts with glycoprotein 130 to promote activation of the IL-6/STAT3 pathway in GSCs. Genetic depletion of CD109 abolished the stemness and self-renewal of GSCs and impaired tumorigenicity. Loss of stemness was accompanied with a phenotypic shift of GSCs to more differentiated astrocytic-like cells. Importantly, genetic or pharmacologic targeting of CD109/STAT3 axis sensitized the GSCs to chemotherapy, suggesting that targeting CD109/STAT3 axis has potential to overcome therapy resistance in glioblastoma.

Indexed as

AnimalsAntigens, CDAntineoplastic Agents, AlkylatingAstrocytomaBrain NeoplasmsCell PlasticityCytokine Receptor gp130Drug Resistance, NeoplasmFemaleGlioblastomaGPI-Linked ProteinsHumansInterleukin-6MaleMiceMice, NudeAntigens, CDAntineoplastic Agents, AlkylatingCD109 protein, humanCytokine Receptor gp130GPI-Linked ProteinsIL6 protein, humanIL6ST protein, humanInterleukin-6Neoplasm ProteinsSTAT3 protein, humanSTAT3 Transcription FactorTemozolomideBrain cancerMolecular biologyMolecular pathologyOncologyStem cells

Identifiers

PMID33986188
PMCPMC8262342
OpenAlexW3161057404

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.