Evidence map›Paper›PMID 32376896›Full record

ArticleScientific reports2020

Catechol inhibits epidermal growth factor-induced epithelial-to-mesenchymal transition and stem cell-like properties in hepatocellular carcinoma cells.

Won-Chul Lim, Hyunhee Kim, Young-Joo Kim, Bu-Nam Jeon, Hee-Bum Kang, Hyeonseok Ko

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 25% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Liver cancer wars: plant-derived polyphenols strike back.Medical oncology (Northwood, London, England) · 2024
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Rose (Molecules (Basel, Switzerland) · 2020
    Article
  15. 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

6 authors at 4 institutions in 1 country.

Won-Chul LimKorea Food Research Institute, Wanju-gun, Jeollabuk-do, Republic of Korea.
Hyunhee KimDepartment of Biomedical Sciences, Asan Medical Center, AMIST, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Young-Joo KimNatural Products Research Center, Korea Institute of Science and Technology, Gangneung, Gangwon-do, Republic of Korea.
Bu-Nam JeonGenome and Company, Pangyo-ro 253, Bundang-gu, Seongnam-si, Gyeonggi-do, Republic of Korea.
Hee-Bum KangVoronoi Research Institute, S 12th F, Songdogwahak-ro 32 (IT center), Yeonsu-gu, Incheon, Republic of Korea.
Hyeonseok KoHLB Life Science, Teheran-ro 420, Gangnam-gu, Seoul, Republic of Korea. drug9054@naver.com.
Genome and Company (South Korea) · KRKorea Food Research Institute · KRKorea Institute of Science and Technology · KRUniversity of Ulsan · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial-mesenchymal transition (EMT) is a major cellular process in which epithelial cells lose cell polarity and cell-cell adhesion and become motility and invasiveness by transforming into mesenchymal cells. Catechol is one of the natural compounds present in fruits and vegetables and has various pharmacological and physiological activities including anti-carcinogenic effects. However, the effects of catechol on EMT has not been reported. Epidermal growth factor (EGF) is one of the growth factors and is known to play a role in inducing EMT. The present study showed that catechol suppressed not only the morphological changes to the mesenchymal phenotype of epithelial HCC cells, but also the reduction of E-cadherin and the increment of Vimentin, which are typical hallmark of EMT. In addition, catechol suppressed EMT-related steps such as migration, invasion, anoikis resistance acquisition, and stem cell-like characterization through the EGFR-AKT-ERK signaling pathway during liver cancer metastasis. Therefore, these results suggest that catechol may be able to regulate the early metastasis of liver cancer in vitro.

Indexed as

Carcinoma, HepatocellularCatecholsCell Line, TumorCell MovementCell ProliferationEnzyme ActivationEpidermal Growth FactorEpithelial-Mesenchymal TransitionErbB ReceptorsGene Expression Regulation, NeoplasticHumansLiver NeoplasmsMatrix Metalloproteinase 2Neoplasm InvasivenessNeoplastic Stem CellsProto-Oncogene Proteins c-aktcatecholCatecholsEpidermal Growth FactorErbB ReceptorsMatrix Metalloproteinase 2Proto-Oncogene Proteins c-aktSnail Family Transcription Factors

Identifiers

PMID32376896
PMCPMC7203133
OpenAlexW3022516675

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.