Evidence map›Paper›PMID 31432165›Full record

ArticleMolecular medicine reports2019

Afatinib, an EGFR inhibitor, decreases EMT and tumorigenesis of Huh‑7 cells by regulating the ERK‑VEGF/MMP9 signaling pathway.

Yafei Chen, Xin Chen, Xiaojun Ding, Yingwei Wang

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

28 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Yafei ChenDepartment of Clinical Laboratory, Tiantai People's Hospital, Taizhou, Zhejiang 317200, P.R. China.
Xin ChenDepartment of Clinical Laboratory, Tiantai People's Hospital, Taizhou, Zhejiang 317200, P.R. China.
Xiaojun DingDepartment of Clinical Laboratory, Tiantai People's Hospital, Taizhou, Zhejiang 317200, P.R. China.
Yingwei WangDepartment of Clinical Laboratory, Tiantai People's Hospital, Taizhou, Zhejiang 317200, P.R. China.
The First People's Hospital of Tianmen · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transcatheter arterial embolization (TAE) therapy has been used in the treatment of inoperable hepatocellular carcinoma (HCC). However, tumor recurrence and metastasis are common in patients after TAE, and these processes may be caused by circulating tumor cells (CTCs). Epithelial‑mesenchymal transition (EMT) serves important roles in CTCs, and abnormal expression and activation of epidermal growth factor receptor (EGFR) is common in cancer cells. Afatinib is an EGFR‑tyrosine kinase inhibitor (TKI). The present study aimed to investigate the effects of afatinib on EMT and tumorigenesis in HCC cells. Western blot analysis suggested that afatinib was able to effectively suppress overactivation of EGFR. Moreover, the expression levels of EMT‑ and metastasis‑associated genes were found to be modulated by afatinib through EGFR inhibition. In addition, Cell Counting Kit‑8 and Transwell assays suggested that the viability, migration and invasion of HCC cells were inhibited by afatinib through EGFR inhibition. Furthermore, the activity of the ERK signaling pathway and the expression levels of vascular endothelial growth factor (VEGF) and matrix metalloproteinase 9 (MMP9) were decreased following treatment with afatinib in vitro. Collectively, the present results suggested that the inhibitory effects of afatinib on EMT and tumorigenesis may be associated with the ERK‑VEGF/MMP9 signaling pathway. The present study provides new insights into understanding the mechanism underlying HCC and may facilitate the development of novel therapeutic strategies to treat HCC recurrence.

Indexed as

AdultAfatinibAgedAged, 80 and overCarcinogenesisCarcinoma, HepatocellularCell Line, TumorEpithelial-Mesenchymal TransitionErbB ReceptorsFemaleHumansLiver NeoplasmsMaleMAP Kinase Signaling SystemMatrix Metalloproteinase 9Middle AgedAfatinibEGFR protein, humanErbB ReceptorsMatrix Metalloproteinase 9MMP9 protein, humanNeoplasm ProteinsVascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID31432165
PMCPMC6755195
OpenAlexW2966621155

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.