Evidence map›Paper›PMID 29234153›Full record

ArticleCancer gene therapy2018

Netrin-1 elicits metastatic potential of non-small cell lung carcinoma cell by enhancing cell invasion, migration and vasculogenic mimicry via EMT induction.

Xiaofei Zhang, Ping Cui, Beichen Ding, Yuening Guo, Kaiyu Han, Jianing Li, Hong Chen, Wei Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Cancer gene therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

23 citing papers in PubMed, 37 citations in OpenAlex.

  1. Molecular mechanisms and therapeutic targets in lung cancer-nerve crosstalk.Chinese medical journal pulmonary and critical care medicine · 2026
    Review
  2. Article
  3. Article
  4. EMT and cancer: what clinicians should know.Nature reviews. Clinical oncology · 2025
    Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Research progress of the netrins and their receptors in cancer.Journal of cellular and molecular medicine · 2024
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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 at 3 institutions in 1 country.

Xiaofei ZhangDepartment of Respiration, The 2nd Affiliated Hospital of Harbin Medical University, Harbin, 150001, P. R. China.
Ping CuiDepartment of Gynaecology, Harbin Medical University Cancer Hospital, Harbin, 150081, P. R. China.
Beichen DingDepartment of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, P. R. China.
Yuening GuoDepartment of Respiration, The First Affiliated Hospital of Harbin Medical University, Harbin, 150001, P. R. China.
Kaiyu HanDepartment of Respiration, The 2nd Affiliated Hospital of Harbin Medical University, Harbin, 150001, P. R. China.
Jianing LiDepartment of Respiration, The 2nd Affiliated Hospital of Harbin Medical University, Harbin, 150001, P. R. China.
Hong ChenDepartment of Respiration, The 2nd Affiliated Hospital of Harbin Medical University, Harbin, 150001, P. R. China.
Wei ZhangDepartment of Respiration, The First Affiliated Hospital of Harbin Medical University, Harbin, 150001, P. R. China. weizhang15har@163.com.
Harbin Medical University · CNFirst Affiliated Hospital of Harbin Medical University · CNTongji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ectopic expression of netrin-1 has been validated in several cancers including non-small cell lung cancer (NSCLC). Recent research confirms the critical role of netrin-1 in NSCLC growth and its prognostic value. Unfortunately, its contribution in NSCLC metastasis remains elusive. Here, netrin-1 had relatively high expression in NSCLC tissues and cells, especially in high metastatic groups. Notably, netrin-1 overexpression aggravated the malignant metastatic behavior of NSCLC cells, including cell invasion, migration, and vasculogenic mimicry (VM), whereas netrin-1 depression reversely dampened the metastatic potential. Mechanism analysis confirmed that elevation of netrin-1 induced the typical morphological changes of epithelial-to-mesenchymal transition (EMT) and increased the expression of EMT markers, including E-cadherin down-regulation and N-cadherin up-regulation. Consistently, netrin-1 inhibition inversely antagonized the occurrence of EMT. Moreover, netrin-1 also activated the oncogenic pathways of PI3K/AKT and ERK signaling. More importantly, blocking these pathways with their antagonists LY294002 or U0126 reversed the effects of netrin-1 overexpression on cell invasion, migration, EMT, and VM formation. Collectively, the current data suggest that netrin-1 can act as a pro-metastatic factor in NSCLC by enhancing cell invasion, migration, and VM via PI3K/AKT and ERK-mediated EMT process, thereby implicating netrin-1 as a novel promising therapeutic target against aggressive NSCLC.

Indexed as

Carcinoma, Non-Small-Cell LungCell MovementEpithelial-Mesenchymal TransitionLung NeoplasmsMAP Kinase Signaling SystemNeovascularization, PathologicA549 CellsFemaleHumansMaleMiddle AgedNeoplasm InvasivenessNeoplasm ProteinsNetrin-1Neoplasm ProteinsNetrin-1NTN1 protein, human

Identifiers

PMID29234153
OpenAlexW2774006753

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.