Evidence map›Paper›PMID 29331415›Full record

ArticleCancer letters2018

Nogo-B receptor promotes epithelial-mesenchymal transition in non-small cell lung cancer cells through the Ras/ERK/Snail1 pathway.

Donghua Wu, Baofeng Zhao, Xiaoyu Qi, Fang Peng, Hailu Fu, Xinming Chi, Qing Robert Miao, Shujuan Shao

Abstract read
In one paragraph

Article in Cancer letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed.

  1. Article
  2. Review
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  17. Article
  18. KRAS K104 modification affects the KRASScientific reports · 2020
    Article
  19. Article
  20. Research advances on neurite outgrowth inhibitor B receptor.Journal of cellular and molecular medicine · 2020
    Review
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

8 authors.

Donghua WuKey Laboratory of Proteomics, Dalian Medical University, Dalian 116044, China.
Baofeng ZhaoCAS Key Laboratory of Separation Sciences for Analytical Chemistry, National Chromatographic R&A Center, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Dalian 116023, China.
Xiaoyu QiDivision of Pediatric Surgery, Department of Surgery, Children's Research Institute, Medical College of Wisconsin, Milwaukee, WI 53226, USA; Divisions of Pediatric Pathology, Department of Pathology, Children's Research Institute, Medical College of Wisconsin, Milwaukee, WI 53226, USA; Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Fang PengKey Laboratory of Proteomics, Dalian Medical University, Dalian 116044, China.
Hailu FuKey Laboratory of Proteomics, Dalian Medical University, Dalian 116044, China.
Xinming ChiKey Laboratory of Proteomics, Dalian Medical University, Dalian 116044, China.
Qing Robert MiaoDivision of Pediatric Surgery, Department of Surgery, Children's Research Institute, Medical College of Wisconsin, Milwaukee, WI 53226, USA; Divisions of Pediatric Pathology, Department of Pathology, Children's Research Institute, Medical College of Wisconsin, Milwaukee, WI 53226, USA; Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI 53226, USA. Electronic address: qmiao@mcw.edu.
Shujuan ShaoKey Laboratory of Proteomics, Dalian Medical University, Dalian 116044, China. Electronic address: shaoshujuan2006@126.com.

Funding

Role of NgBRR01HL108938 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI MIAO, QING · 2011 to 2015
$1.8M
NHLBI NIH HHS R01 HL108938
6 · The paper itself

Abstract

Nogo-B receptor (NgBR) is a specific receptor of Nogo-B that regulates vascular remodeling and angiogenesis. Previously, we found that NgBR promotes the membrane translocation and activation of Ras in breast cancer cells and enhances the chemoresistance of hepatocellular carcinoma cells to 5-fluorouracil. However, the role of NgBR in lung cancer has not yet been elucidated. In the present study, we found that NgBR knockdown inhibited epithelial-mesenchymal transition (EMT) in non-small cell lung cancer (NSCLC) cells in vitro and metastasis of NSCLC cells in vivo. In contrast, NgBR overexpression promoted EMT in and lung metastasis of NSCLC cells. At the molecular level, NgBR modulated the expression of EMT-related proteins and enhanced the protein expression of Snail1, a crucial transcription factor that represses epithelial cell protein marker E-cadherin. Moreover, we found that NgBR overexpression promoted the membrane localization of Ras and activation of downstream MEK/ERK signaling pathway and that NgBR knockdown by using a specific shRNA inversely affected the expression of EMT-related proteins in NSCLC cells. Thus, our results provide novel insights on the regulatory role of NgBR in the metastasis of NSCLC that should be investigated further for developing a therapeutic strategy for treating patients with NSCLC.

Indexed as

A549 CellsAnimalsCarcinoma, Non-Small-Cell LungCell Line, TumorEpithelial-Mesenchymal TransitionExtracellular Signal-Regulated MAP KinasesGene Expression Regulation, NeoplasticHumansLung NeoplasmsMaleMice, Inbred BALB CMice, NudeNeoplasm Metastasisras ProteinsReceptors, Cell SurfaceRNA InterferenceExtracellular Signal-Regulated MAP KinasesNUS1 protein, humanras ProteinsReceptors, Cell SurfaceSNAI1 protein, humanSnail Family Transcription FactorsEpithelial–mesenchymal transitionMetastasisNogo-B receptorNon-small cell lung cancerSnail1

Identifiers

PMID29331415
PMCPMC7385903

What OpenQuestion holds

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Registered trials

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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.