Evidence map›Paper›PMID 22829019›Full record

ArticleMolecular and cellular biochemistry2012

Long-term exposure to imatinib reduced cancer stem cell ability through induction of cell differentiation via activation of MAPK signaling in glioblastoma cells.

Yucui Dong, Qinglian Han, Yan Zou, Zhenling Deng, Xinliang Lu, Xiaohua Wang, Weihua Zhang, Hua Jin, Jun Su, Tao Jiang and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 49 citations in OpenAlex.

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  11. PamInvestigational new drugs · 2020
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  14. The function of BTG3 in colorectal cancer cells and its possible signaling pathway.Journal of cancer research and clinical oncology · 2018
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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

11 authors at 4 institutions in 1 country.

Yucui DongDepartment of Immunology, Harbin Medical University, Harbin, China.
Qinglian Han
Yan Zou
Zhenling Deng
Xinliang Lu
Xiaohua Wang
Weihua Zhang
Hua Jin
Jun Su
Tao Jiang
Huan Ren
Harbin Medical University · CNThird Affiliated Hospital of Harbin Medical University · CNBeijing Institute of Neurosurgery · CNEducation Department of Heilongjiang Province · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) was shown to harbor therapy-resistant cancer stem cells that were major causes of recurrence. PDGFR (platelet-derived growth factor receptor) and c-Kit (stem cell factor receptor) signaling play important roles in initiation and maintenance of malignant glioma. This study demonstrated that long-term culture with imatinib mesylate, the tyrosine kinase inhibitor against PDGFR and c-Kit resulted in reduced cancer stem cell ability in glioblastoma cells through cell differentiation. Derived from RG glioblastoma cells co-cultured with imatinib for 3 months, RG-IM cells showed distinct properties of cell cycle distribution and morphology in addition to significantly decreased ability to form aggregates and colonies in vitro and tumorigenicity in vivo. Increased expression of GFAP (astrocyte marker) and class III β-tubulin isotype (Tuj1, neuron marker) were detected with morphology like neurons or astrocytes in RG-IM cells. Furthermore, decreased expression of stem cell markers, i.e., CD133, Oct-3/4, nestin, and Bmi1, and increased terminal neural cell markers, GFAP, Tuj1, etc., were identified in RG-IM at the mRNA level. All these markers were changed in RG cells when PDGFRB and c-Kit expression were double knocked down by siRNA. Cell differentiation agent, all-trans retinoic acid (ATRA) caused similar effect as that with imatinib in RG cells, while adding PDGF-B and SCF in RG-IM resulted in cell dedifferentiation to some extent. Moreover, differentiation in RG cells treated by imatinib or ATRA was mainly driven by MAPK signaling pathways. In summary, continuous inhibition on PDGFR and c-Kit signaling disturbed glioma stem cells biology in subsets of GBM cells and may have potentials in clinical applications.

Indexed as

AnimalsBenzamidesCell DifferentiationCell Line, TumorCell Transformation, NeoplasticEnzyme ActivationGene Expression Regulation, NeoplasticGlioblastomaHumansImatinib MesylateMAP Kinase Signaling SystemMiceMice, NudeNeoplastic Stem CellsPiperazinesProto-Oncogene Proteins c-kitBenzamidesImatinib MesylatePiperazinesProto-Oncogene Proteins c-kitPyrimidinesReceptors, Platelet-Derived Growth Factor

Identifiers

PMID22829019
OpenAlexW1967578658

What OpenQuestion holds

Textmetadata
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.