Evidence map›Paper›PMID 29254230›Full record

ArticleOncotarget2017

MiR-29b/TET1/ZEB2 signaling axis regulates metastatic properties and epithelial-mesenchymal transition in breast cancer cells.

Hua Wang, Xinglan An, Hao Yu, Sheng Zhang, Bo Tang, Xueming Zhang, Ziyi Li

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 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

34 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Mechanisms that regulate the activities of TET proteins.Cellular and molecular life sciences : CMLS · 2022
    Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. The Roles of DNA Demethylases in Triple-Negative Breast Cancer.Pharmaceuticals (Basel, Switzerland) · 2021
    Review
  16. CEA, CA 15-3, and miRNA expression as potential biomarkers in canine mammary tumors.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2021
    Article
  17. Article
  18. Review
  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

7 authors at 2 institutions in 1 country.

Hua Wang *The First Bethune Hospital, Jilin University, Changchun, Jilin 130021, China.
Xinglan An *The First Bethune Hospital, Jilin University, Changchun, Jilin 130021, China.
Hao YuCollege of Animal Science, Jilin University, Changchun, Jilin 130062, China.
Sheng ZhangThe First Bethune Hospital, Jilin University, Changchun, Jilin 130021, China.
Bo TangCollege of Veterinary Medicine, Jilin University, Changchun, Jilin 130062, China.
Xueming ZhangCollege of Veterinary Medicine, Jilin University, Changchun, Jilin 130062, China.
Ziyi LiThe First Bethune Hospital, Jilin University, Changchun, Jilin 130021, China.
First Bethune Hospital of Jilin University · CNJilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MiR-29b has been reported to be both a suppressor and a promoter in breast cancer (BC) cells proliferation and metastasis. Significant efforts have been made to explain the seemingly contradictory effects of miR-29b on BC, but no answer has yet been clearly verified. In this study, we overexpressed and knocked down miR-29b in BC cell lines, modulated expression of its downstream target gene TET1 and downregulated a downstream target gene of TET1, ZEB2, to explore the regulatory mechanism of miR-29b in BC cell proliferation, migration and epithelial-mesenchymal transition (EMT). Our results showed lower expression of miR-29b in BC samples and cell lines. Functional assays showed that miR-29b overexpression resulted in a higher cell proliferation, greater colony formation, higher migration rate and EMT. A dual luciferase assay identified TET1 as a direct target of miR-29b. As the promoting effects of miR-29b in the proliferation and metastasis of MDA-MB-231 and MCF-7, knockdown of TET1 also led to increased proliferation, colony formation, invasion and EMT. Further, we found that TET1 bound to the promoter of ZEB2, and siTET1 enhanced ZEB2 expression. Disruption of ZEB2 expression inhibited BC cells proliferation, colony formation and invasion. Our results establish the miR-29b/TET1/ZEB2 pathway in BC cell proliferation, migration and provide a theoretical basis for further research on the molecular mechanisms and new clinical treatments for BC.

Indexed as

breast cancermetastasisMiR-29bTET1ZEB2

Identifiers

PMID29254230
PMCPMC5731940
OpenAlexW2766649156

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.