Evidence map›Paper›PMID 30755817›Full record

ArticleAmerican journal of cancer research2019

Dysregulated ENPP1 increases the malignancy of human lung cancer by inducing epithelial-mesenchymal transition phenotypes and stem cell features.

Min Hu, Wenzheng Guo, Yueling Liao, Dongliang Xu, Beibei Sun, Hongyong Song, Tong Wang, Yanbin Kuang, Bo Jing, Kaimi Li and 3 more

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.2field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. ENPP1 is an innate immune checkpoint of the anticancer cGAMP-STING pathway in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  10. ENPP1 Immunobiology as a Therapeutic Target.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. AnCancer informatics · 2022
    Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. PTGES/PGEOncogene · 2020
    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

13 authors at 4 institutions in 2 countries.

Min HuKey Laboratory of Cell Differentiation and Apoptosis of Chinese Minister of Education, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine Shanghai, China.
Wenzheng GuoDepartment of Laboratory Medicine, Shanghai East Hospital, Tongji University School of Medicine Shanghai, China.
Yueling LiaoKey Laboratory of Cell Differentiation and Apoptosis of Chinese Minister of Education, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine Shanghai, China.
Dongliang XuKey Laboratory of Cell Differentiation and Apoptosis of Chinese Minister of Education, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine Shanghai, China.
Beibei SunTranslational Medical Research Center, Shanghai Jiao Tong University Shanghai, China.
Hongyong SongKey Laboratory of Cell Differentiation and Apoptosis of Chinese Minister of Education, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine Shanghai, China.
Tong WangKey Laboratory of Cell Differentiation and Apoptosis of Chinese Minister of Education, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine Shanghai, China.
Yanbin KuangDepartment of Respiratory Medicine, The Second Affiliated Hospital, Dalian Medical University Dalian, China.
Bo JingKey Laboratory of Cell Differentiation and Apoptosis of Chinese Minister of Education, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine Shanghai, China.
Kaimi LiKey Laboratory of Cell Differentiation and Apoptosis of Chinese Minister of Education, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine Shanghai, China.
Jing LingDepartment of Oncology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine Shanghai, China.
Feng YaoDepartment of Thoracic Surgery, Shanghai Chest Hospital, Shanghai Jiao Tong University Shanghai, China.
Jiong DengKey Laboratory of Cell Differentiation and Apoptosis of Chinese Minister of Education, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine Shanghai, China.
Shanghai Jiao Tong University · CNDalian Medical University · CNShanghai Chest Hospital · CNShanghai East Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Induction of cancer stem cell (CSC) characters and epithelial mesenchymal transition (EMT) features are crucial in tumor initiation, progression and metastasis. However, underlying mechanisms remain incompletely understood. Here, we showed that ENPP1 plays an important role in inducing and maintaining EMT phenotypes and CSC features in lung cancer. ENPP1 is upregulated in lung cancer cells. ENPP1-knockdown in lung cancer HCC827 cells and A549 cells resulted in suppressed colonogenic formation, anchorage-independent growth in vitro, and tumorigenicity in vivo. ENPP1-knockdown also reduced expression of CSC makers, including ABCG2, SOX2, NANOG, and CD44. Moreover, ENPP1-knockdown reversed TGFβ-induced EMT phenotypes, including cell migration, E-cadherin repression and vimentin induction. Finally, upregulated ENPP1 was identified in majority of human lung tumor tissues compared to adjacent normal lung tissues. Taken together, our study demonstrates that dysregulated ENPP1 contributes to increased malignancy of human lung cancer by inducing CSC-features, and EMT-like phenotypes.

Indexed as

EMTENPP1lung cancermigrationstemness

Identifiers

PMID30755817
PMCPMC6356920
OpenAlexW2980402366

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.