Evidence map›Paper›PMID 24621612›Full record

ArticlePloS one2014

DLK1 promotes lung cancer cell invasion through upregulation of MMP9 expression depending on Notch signaling.

Lin Li, Jinjing Tan, Ying Zhang, Naijun Han, Xuebing Di, Ting Xiao, Shujun Cheng, Yanning Gao, Yu Liu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

42 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. LncRNAs in theInternational journal of molecular sciences · 2024
    Article
  3. Article
  4. Article
  5. A functionalFrontiers in medicine · 2023
    Article
  6. Frontiers in immunology · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Emerging Roles of DLK1 in the Stem Cell Niche and Cancer Stemness.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2022
    Review
  13. Article
  14. Niche-derived soluble DLK1 promotes glioma growth.Neoplasia (New York, N.Y.) · 2020
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  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

9 authors at 1 institution in 1 country.

Lin LiState Key Laboratory of Molecular Oncology, Department of Etiology and Carcinogenesis, Cancer Institute (Hospital), Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing, P. R. China.
Jinjing TanState Key Laboratory of Molecular Oncology, Department of Etiology and Carcinogenesis, Cancer Institute (Hospital), Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing, P. R. China.
Ying ZhangState Key Laboratory of Molecular Oncology, Department of Etiology and Carcinogenesis, Cancer Institute (Hospital), Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing, P. R. China.
Naijun HanState Key Laboratory of Molecular Oncology, Department of Etiology and Carcinogenesis, Cancer Institute (Hospital), Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing, P. R. China.
Xuebing DiState Key Laboratory of Molecular Oncology, Department of Etiology and Carcinogenesis, Cancer Institute (Hospital), Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing, P. R. China.
Ting XiaoState Key Laboratory of Molecular Oncology, Department of Etiology and Carcinogenesis, Cancer Institute (Hospital), Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing, P. R. China.
Shujun ChengState Key Laboratory of Molecular Oncology, Department of Etiology and Carcinogenesis, Cancer Institute (Hospital), Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing, P. R. China.
Yanning GaoState Key Laboratory of Molecular Oncology, Department of Etiology and Carcinogenesis, Cancer Institute (Hospital), Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing, P. R. China.
Yu LiuState Key Laboratory of Molecular Oncology, Department of Etiology and Carcinogenesis, Cancer Institute (Hospital), Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing, P. R. China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transmembrane and secreted protein delta-like 1 homolog (DLK1) belongs to the EGF-like family. It is widely accepted that DLK1 plays important roles in regulating cell differentiation, such as adipogenesis and osteogenesis. Aberrant expression of DLK1 has been found in various types of human cancers, including lung cancer. A previous study in this lab has revealed that DLK1 is associated with tumor invasion, although the mechanism is still unknown. To explore the potential effects that DLK1 might have on invasion, DLK1 was overexpressed or knocked down in the human lung cancer cell lines. The protein's influences on cell invasion were subsequently evaluated. A transwell assay showed that DLK1 overexpression significantly promoted cancer cell invasion. Western blotting and gelatin zymography analysis indicated that DLK1 could affect both matrix metalloproteinase-9 (MMP9) expression and its extracellular activity. An analysis of NOTCH1 and HES1 gene expression and Notch intracellular domain (NICD) nuclear translocation during DLK1 stimulation or depletion demonstrated that DLK1 could activate Notch signaling in lung cancer cells. Additionally, the elevated expression of MMP9 induced by DLK1 stimulation could be significantly decreased by inhibiting Notch signaling using γ-secretase inhibitor (GSI). The data presented in this study suggest that DLK1 can promote the invasion of lung cancer cells by upregulating MMP9 expression, which depends on Notch signaling.

Indexed as

Signal TransductionUp-RegulationCalcium-Binding ProteinsCell Line, TumorExtracellular MatrixHumansIntercellular Signaling Peptides and ProteinsLung NeoplasmsMatrix Metalloproteinase 9Membrane ProteinsNeoplasm InvasivenessReceptors, NotchCalcium-Binding ProteinsDLK1 protein, humanIntercellular Signaling Peptides and ProteinsMatrix Metalloproteinase 9Membrane ProteinsReceptors, Notch

Identifiers

PMID24621612
PMCPMC3951400
OpenAlexW2019041344

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.