Evidence map›Paper›PMID 27602960›Full record

ArticleOncotarget2016

Endothelin-1 promotes epithelial-mesenchymal transition in human chondrosarcoma cells by repressing miR-300.

Min-Huan Wu, Pei-Han Huang, Mingli Hsieh, Chun-Hao Tsai, Hsien-Te Chen, Chih-Hsin Tang

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 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Burns & trauma · 2025
    Article
  5. Endothelin and the tumor microenvironment: a finger in every pie.Clinical science (London, England : 1979) · 2024
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. MicroRNAs in Bone Metastasis.Current osteoporosis reports · 2019
    Review
  13. Article
  14. Article
  15. MicroRNA-1 acts as a tumor suppressor microRNA by inhibiting angiogenesis-related growth factors in human gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2018
    Article
  16. Article
  17. 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.

Min-Huan WuPhysical Education Office, Tunghai University, Taichung, Taiwan.
Pei-Han HuangGraduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan.
Mingli HsiehDepartment of Life Science, Tunghai University, Taichung, Taiwan.
Chun-Hao TsaiDepartment of Orthopedic Surgery, China Medical University Hospital, Taichung, Taiwan.
Hsien-Te ChenDepartment of Orthopedic Surgery, China Medical University Hospital, Taichung, Taiwan.
Chih-Hsin TangGraduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan.
China Medical University · TWChina Medical University Hospital · TWTunghai University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chondrosarcoma is a malignant tumor of mesenchymal origin predominantly composed of cartilage-producing cells. This type of bone cancer is extremely resistant to radiotherapy and chemotherapy. Surgical resection is the primary treatment, but is often difficult and not always practical for metastatic disease, so more effective treatments are needed. In particular, it would be helpful to identify molecular markers as targets for therapeutic intervention. Endothelin-1 (ET-1), a potent vasoconstrictor, has been shown to enhance chondrosarcoma angiogenesis and metastasis. We report that ET-1 promotes epithelial-mesenchymal transition (EMT) in human chondrosarcoma cells. EMT is a key pathological event in cancer progression, during which epithelial cells lose their junctions and apical-basal polarity and adopt an invasive phenotype. Our study verifies that ET-1 induces the EMT phenotype in chondrosarcoma cells via the AMP-activated protein kinase (AMPK) pathway. In addition, we show that ET-1 increases EMT by repressing miR-300, which plays an important role in EMT-enhanced tumor metastasis. We also show that miR-300 directly targets Twist, which in turn results in a negative regulation of EMT. We found a highly positive correlation between ET-1 and Twist expression levels as well as tumor stage in chondrosarcoma patient specimens. Therefore, ET-1 may represent a potential novel molecular therapeutic target in chondrosarcoma metastasis.

Indexed as

3' Untranslated RegionsAMP-Activated Protein KinasesBone NeoplasmsCell Line, TumorCell MovementChondrosarcomaEndothelin-1Epithelial-Mesenchymal TransitionHumansMicroRNAsNuclear ProteinsReceptors, EndothelinTwist-Related Protein 13' Untranslated RegionsAMP-Activated Protein KinasesEndothelin-1MicroRNAsMIRN300 microRNA, humanNuclear ProteinsReceptors, EndothelinTWIST1 protein, humanTwist-Related Protein 1AMPKendothelin-1epithelial to mesenchymal transitionmiR-300Twist

Identifiers

PMID27602960
PMCPMC5342549
OpenAlexW2517794445

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.