Evidence map›Paper›PMID 29100291›Full record

ArticleOncotarget2017

Hinokitiol up-regulates miR-494-3p to suppress BMI1 expression and inhibits self-renewal of breast cancer stem/progenitor cells.

Shih-Ming Chen, Bing-Yen Wang, Che-Hsin Lee, Hsueh-Te Lee, Jung-Jung Li, Guan-Ci Hong, Yu-Chieh Hung, Peng-Ju Chien, Che-Ying Chang, Li-Sung Hsu and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

30 citing papers in PubMed, 51 citations in OpenAlex.

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

11 authors at 4 institutions in 1 country.

Shih-Ming ChenInstitute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, Taiwan.
Bing-Yen WangDivision of Thoracic Surgery, Department of Surgery, Changhua Christian Hospital, Changhua City, Taiwan.
Che-Hsin LeeDepartment of Biological Sciences, National Sun Yat-sen University, Kaohsiung, Taiwan.
Hsueh-Te LeeInstitute of Anatomy and Cell Biology, School of Medicine, National Yang Ming University, Taipei City, Taiwan.
Jung-Jung LiDepartment of Biomedical Sciences, Chung Shan Medical University, Taichung, Taiwan.
Guan-Ci HongDepartment of Biomedical Sciences, Chung Shan Medical University, Taichung, Taiwan.
Yu-Chieh HungDepartment of Biomedical Sciences, Chung Shan Medical University, Taichung, Taiwan.
Peng-Ju ChienDepartment of Biomedical Sciences, Chung Shan Medical University, Taichung, Taiwan.
Che-Ying ChangDepartment of Biomedical Sciences, Chung Shan Medical University, Taichung, Taiwan.
Li-Sung HsuInstitute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, Taiwan.
Wen-Wei ChangDepartment of Biomedical Sciences, Chung Shan Medical University, Taichung, Taiwan.
Chung Shan Medical University · TWKaohsiung Medical University · TWNational Sun Yat-sen University · TWNational Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hinokitiol (β-thujaplicin) is a tropolone-related compound that has anti-microbe, anti-inflammation, and anti-tumor effects. Cancer stem/progenitor cells (CSCs) are a subpopulation of cancer cells with tumor initiation, chemoresistant, and metastatic properties and have been considered the important therapeutic target in future cancer therapy. Previous studies reported that hinokitiol exhibits an anti-cancer activity against murine tumor cells through the induction of autophagy. The current research revealed that hinokitiol suppressed the self-renewal capabilities of human breast CSCs (BCSCs) and inhibited the expression of BMI1 at protein level without suppressing its mRNA. Treatment of hinokitiol in mammospheres induced the expression of miR-494-3p and inhibition of miR-494-3p expression in BCSCs. This treatment abolished the suppressive effects of hinokitiol in mammosphere formation and BMI1 expression. BMI1 is a target of miR-494-3p by luciferase-based 3'UTR reporter assay. Overexpression of miR-494-3p in BCSCs caused the down-regulation of BMI1 protein, inhibition of mammosphere forming capability, and suppression of their tumorigenicity. Moreover, miR-494-3p expression was significantly and inversely correlated with patient survival in two independent public database sets. Furthermore, treatment of hinokitiol

Indexed as

BMI1breast cancercancer stem cellshinokitiolmiR-494-3p

Identifiers

PMID29100291
PMCPMC5652685
OpenAlexW2727403160

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.