Evidence map›Paper›PMID 25204555›Full record

ArticleNeuro-oncology2015

PTK7 regulates Id1 expression in CD44-high glioma cells.

Qing Liu, Chi Zhang, Jian Yuan, Jun Fu, Minghua Wu, Jun Su, Xiangyu Wang, Xianrui Yuan, Weixi Jiang

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuro-oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 31% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
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  12. [Increased TRIM5 is associated with a poor prognosis and immune infiltration in glioma patients].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2020
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  15. Inhibitor of Differentiation 1 (Id1) in Cancer and Cancer Therapy.International journal of medical sciences · 2020
    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

9 authors at 1 institution in 1 country.

Qing LiuDepartment of Neurosurgery, Central South University, Hunan, China (Q.L, C.Z., J.Y., J.F., J.S., X.W., X.Y., W.J.); The Institute of Skull Base Surgery and Neurooncology at Hunan, China (Q.L., J.Y., J.F., X.Y., W.J.); Cancer Research Institute, Central South University, Hunan, China (M.W.).
Chi ZhangDepartment of Neurosurgery, Central South University, Hunan, China (Q.L, C.Z., J.Y., J.F., J.S., X.W., X.Y., W.J.); The Institute of Skull Base Surgery and Neurooncology at Hunan, China (Q.L., J.Y., J.F., X.Y., W.J.); Cancer Research Institute, Central South University, Hunan, China (M.W.).
Jian YuanDepartment of Neurosurgery, Central South University, Hunan, China (Q.L, C.Z., J.Y., J.F., J.S., X.W., X.Y., W.J.); The Institute of Skull Base Surgery and Neurooncology at Hunan, China (Q.L., J.Y., J.F., X.Y., W.J.); Cancer Research Institute, Central South University, Hunan, China (M.W.).
Jun FuDepartment of Neurosurgery, Central South University, Hunan, China (Q.L, C.Z., J.Y., J.F., J.S., X.W., X.Y., W.J.); The Institute of Skull Base Surgery and Neurooncology at Hunan, China (Q.L., J.Y., J.F., X.Y., W.J.); Cancer Research Institute, Central South University, Hunan, China (M.W.).
Minghua WuDepartment of Neurosurgery, Central South University, Hunan, China (Q.L, C.Z., J.Y., J.F., J.S., X.W., X.Y., W.J.); The Institute of Skull Base Surgery and Neurooncology at Hunan, China (Q.L., J.Y., J.F., X.Y., W.J.); Cancer Research Institute, Central South University, Hunan, China (M.W.).
Jun SuDepartment of Neurosurgery, Central South University, Hunan, China (Q.L, C.Z., J.Y., J.F., J.S., X.W., X.Y., W.J.); The Institute of Skull Base Surgery and Neurooncology at Hunan, China (Q.L., J.Y., J.F., X.Y., W.J.); Cancer Research Institute, Central South University, Hunan, China (M.W.).
Xiangyu WangDepartment of Neurosurgery, Central South University, Hunan, China (Q.L, C.Z., J.Y., J.F., J.S., X.W., X.Y., W.J.); The Institute of Skull Base Surgery and Neurooncology at Hunan, China (Q.L., J.Y., J.F., X.Y., W.J.); Cancer Research Institute, Central South University, Hunan, China (M.W.).
Xianrui YuanDepartment of Neurosurgery, Central South University, Hunan, China (Q.L, C.Z., J.Y., J.F., J.S., X.W., X.Y., W.J.); The Institute of Skull Base Surgery and Neurooncology at Hunan, China (Q.L., J.Y., J.F., X.Y., W.J.); Cancer Research Institute, Central South University, Hunan, China (M.W.).
Weixi JiangDepartment of Neurosurgery, Central South University, Hunan, China (Q.L, C.Z., J.Y., J.F., J.S., X.W., X.Y., W.J.); The Institute of Skull Base Surgery and Neurooncology at Hunan, China (Q.L., J.Y., J.F., X.Y., W.J.); Cancer Research Institute, Central South University, Hunan, China (M.W.).
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCD44 is a molecular marker associated with molecular subtype and treatment resistance in glioma. More effective therapies will result from approaches aimed at targeting the CD44-high gliomas.

methodsProtein tyrosine kinase 7 (PTK7) mRNA expression was analyzed based on The Cancer Genome Atlas glioblastoma dataset. PTK7 expression was depleted through lentivirus-mediated short hairpin RNA knockdown. Terminal deoxynucleotidyl transferase dUTP nick-end labeling was used to evaluate cell apoptosis following PTK7 knockdown. Gene expression analysis was performed on Affymetrix microarray. A nude mice orthotopic tumor model was used to evaluate the in vivo effect of PTK7 depletion.

resultsPTK7 is highly expressed in CD44-high glioblastoma and predicts unfavorable prognosis. PTK7 knockdown attenuated cell proliferation, impaired tumorigenic potential, and induced apoptosis in CD44-high glioma cell lines. Gene expression analysis identified inhibitor of DNA Binding 1 (Id1) gene as a potential downstream effector for PTK7. Overexpression of Id1 mostly restored the cell proliferation and colony formation attenuated by PTK7 depletion. PTK7 enhanced anchorage-independent growth in normal human astrocytes, which was attenuated by Id1 knockdown. Furthermore, PTK7 regulated Id1 expression through modulating TGF-β/Smad signaling, while pharmacological inhibition on TGF-β/Smad signaling or PTK7/Id1 depletion attenuated TGF-β-stimulated cell proliferation. PTK7 depletion consistently reduced Id1 expression, suppressed tumor growth, and induced apoptosis in a murine orthotopic tumor model, which could be translated into prolonged survival in tumor-bearing mice.

conclusionsPTK7 regulates Id1 expression in CD44-high glioma cell lines. Targeting PTK7 could be an effective strategy for treating glioma with high CD44 expression.

Indexed as

AnimalsAntibodiesApoptosisBiomarkersBrain NeoplasmsCell Adhesion MoleculesCell Line, TumorCell ProliferationGene ExpressionGlioblastomaHumansHyaluronan ReceptorsInhibitor of Differentiation Protein 1Kaplan-Meier EstimateMiceMice, NudeAntibodiesBiomarkersCD44 protein, humanCell Adhesion MoleculesHyaluronan ReceptorsID1 protein, humanInhibitor of Differentiation Protein 1PTK7 protein, humanReceptor Protein-Tyrosine KinasesCD44cell proliferationgliomaPTK7tumorigenesis

Identifiers

PMID25204555
PMCPMC4483067
OpenAlexW2084221469

What OpenQuestion holds

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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.