Evidence map›Paper›PMID 24682943›Full record

ArticleJournal of molecular neuroscience : MN2015

Nucleolin promotes TGF-β signaling initiation via TGF-β receptor I in glioblastoma.

Shunzeng Lv, Jie Zhang, Mingzhi Han, Weiping Wang, Ya Zhang, Dongxiao Zhuang, Ranran Shi, Ruixiang Bian, Chengjun Yao

RetractedAbstract readRetracted Publication
PubMed Publisher
In one paragraph

Article in Journal of molecular neuroscience : MN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

9 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Evaluation of rs1982073 polymorphism of transforming growth factor-β1 in glioblastoma.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2019
    Article
  5. Article
  6. Review
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  8. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Shunzeng LvPeking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Jie ZhangPeking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Mingzhi HanShandong University School of Medicine, Jinan, Shandong, China.
Weiping WangDepartment of Radiotherapy, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Ya ZhangShandong University School of Medicine, Jinan, Shandong, China.
Dongxiao ZhuangGlioma Surgery Division, Neurological Surgery Department, Huashan Hospital, Shanghai Medical College of Fudan University, Shanghai, China, 200040.
Ranran ShiShandong University School of Medicine, Jinan, Shandong, China.
Ruixiang BianShandong University School of Medicine, Jinan, Shandong, China.
Chengjun YaoGlioma Surgery Division, Neurological Surgery Department, Huashan Hospital, Shanghai Medical College of Fudan University, Shanghai, China, 200040. cjyhuashan@163.com.
Shandong University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNShanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transforming growth factor β (TGF-β) pathway plays a key role in oncogenesis of advanced cancers, involving the non-Smad and Smad pathways. Meanwhile, nucleolin on the cell surface has been also reported to affect activation of signaling pathways. However, the effect of cell surface nucleolin on TGF-β pathway in glioblastoma is not still understood. Here, using antibodies of nucleolin and TGF-β receptor I (TβR-I), we observed blocking of either nucleolin or TβR-I inhibited the phosphorylation of CrkL, Erk1/2, and Smad2. Using nucleolin siRNA, nucleolin knockdown was also identified to suppress the expression of p-CrkL, p-Erk1/2, and p-Smad2. Furthermore, immunoprecipitation revealed the interaction between cell surface nucleolin and TβR-I on the U87 cell membrane. In addition, U87 cell wound-healing, soft-agar and MTT assay also showed si-nucleolin could obviously impair wound closure (p < 0.001), colony formation (p < 0.001) and cell growth (p < 0.001). In conclusion, nucleolin promotes and regulates the TGF-β pathway by interacting with TβR-I and is required for initiation and activation of TGF-β signaling. Thus, nucleolin could be a key factor in glioblastoma pathogenesis and considered a therapeutic target, which may also mediate more signaling pathways.

Indexed as

MAP Kinase Signaling SystemAdaptor Proteins, Signal TransducingCell Line, TumorCell MovementCell ProliferationGlioblastomaHumansMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Nuclear ProteinsNucleolinPhosphoproteinsProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IRNA-Binding ProteinsAdaptor Proteins, Signal TransducingCRKL proteinMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Nuclear ProteinsNucleolinPhosphoproteinsProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IRNA-Binding ProteinsSmad2 ProteinTransforming Growth Factor beta

Identifiers

PMID24682943
OpenAlexW2911385888

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.