Evidence map›Paper›PMID 27145282›Full record

ArticleOncotarget2016

Inhibition of cancer cell epithelial mesenchymal transition by normal fibroblasts via production of 5-methoxytryptophan.

Huei-Hsuan Cheng, Ling-Yun Chu, Li-Yi Chiang, Hua-Ling Chen, Cheng-Chin Kuo, Kenneth K Wu

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 22% 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

12 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Cytoguardin: A Tryptophan Metabolite against Cancer Growth and Metastasis.International journal of molecular sciences · 2021
    Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Restoration of hydroxyindoleThe Journal of biological chemistry · 2018
    Article
  12. 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 3 institutions in 1 country.

Huei-Hsuan ChengMetabolomic Medicine Research Center, China Medical University Hospital, Taichung, Taiwan.
Ling-Yun ChuMetabolomic Medicine Research Center, China Medical University Hospital, Taichung, Taiwan.
Li-Yi ChiangMetabolomic Medicine Research Center, China Medical University Hospital, Taichung, Taiwan.
Hua-Ling ChenInstitute of Cellular and System Medicine, National Health Research Institutes, Zhunan, Taiwan.
Cheng-Chin KuoGraduate Institute of Clinical Medical Science, China Medical University, Taichung, Taiwan.
Kenneth K WuMetabolomic Medicine Research Center, China Medical University Hospital, Taichung, Taiwan.
China Medical University Hospital · TWNational Health Research Institutes · TWChina Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We reported previously that human fibroblasts release 5-methoxytryptophan (5-MTP) which inhibits cancer cell COX-2 overexpression and suppresses cancer cell migration and metastasis. To determine whether fibroblasts block cancer cell epithelial mesenchymal transition (EMT) via 5-MTP, we evaluated the effect of Hs68 fibroblasts (HsFb) on A549 cancer cell EMT in a two-chamber system. Co-incubation of A549 with HsFb prevented TGF-β1-induced reduction of E-cadherin and increase in Snail and N-cadherin. Transfection of HsFb with tryptophan hydroxylase-1 siRNA, which inhibited tryptophan hydroxylase-1 protein expression and 5-MTP release in HsFb abrogated the effect of HsFb on A549 EMT. Direct addition of pure 5-MTP to cultured A549 cells followed by TGF-β1 prevented TGF-β1-induced reduction of E-cadherin, and elevation of Snail, vimentin and matrix metalloproteinase 9. Administration of 5-MTP to a murine xenograft tumor model reduced vimentin protein expression in the tumor tissues compared to vehicle control which was correlated with reduction of metastasis in the 5-MTP treated mice. Our experimental data suggest that 5-MTP exerted its anti-EMT actions through inhibition of p38 MAPK activation, p65/p50 NF-κB nuclear translocation and transactivation without the involvement of COX-2 or p300 histone acetyltransferase. Our findings indicate that fibroblasts release a tryptophan metabolite, 5-MTP, to reduce cancer cell EMT, migration, invasion and metastasis.

Indexed as

Xenograft Model Antitumor AssaysA549 CellsAnimalsCadherinsCell LineCoculture TechniquesEpithelial-Mesenchymal TransitionFibroblastsHumansLung NeoplasmsMice, SCIDNF-kappa Bp38 Mitogen-Activated Protein KinasesRNA InterferenceTransforming Growth Factor beta1Tryptophan5-methoxytryptophanCadherinsNF-kappa Bp38 Mitogen-Activated Protein KinasesTph1 protein, mouseTransforming Growth Factor beta1TryptophanTryptophan HydroxylaseVimentin5-methoxytryptophanepithelial mesenchymal transitionfibroblastslung cancertryptophan hydroxylase-1

Identifiers

PMID27145282
PMCPMC5058753
OpenAlexW2344113909

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.