Evidence map›Paper›PMID 27065318›Full record

ArticleOncogene2016

miR-155 downregulates ErbB2 and suppresses ErbB2-induced malignant transformation of breast epithelial cells.

X-H He, W Zhu, P Yuan, S Jiang, D Li, H-W Zhang, M-F Liu

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

37 citing papers in PubMed, 44 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. HDAC2 as a target for developing anti-cancer drugs.Computational and structural biotechnology journal · 2023
    Review
  11. Article
  12. Article
  13. Article
  14. MicroRNAs in Leukemias: A Clinically Annotated Compendium.International journal of molecular sciences · 2022
    Article
  15. Review
  16. Article
  17. Observational
  18. Review
  19. Article
  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 6 institutions in 1 country.

X-H HeCenter for RNA Research, State Key Laboratory of Molecular Biology-University of Chinese Academy of Sciences, CAS Center for Excellence in Molecular Cell Science, Shanghai, China.
W ZhuDepartment of General Surgery, Zhongshan Hospital Affiliated to Fudan University, Shanghai, China.
P YuanCenter for RNA Research, State Key Laboratory of Molecular Biology-University of Chinese Academy of Sciences, CAS Center for Excellence in Molecular Cell Science, Shanghai, China.
S JiangCenter for RNA Research, State Key Laboratory of Molecular Biology-University of Chinese Academy of Sciences, CAS Center for Excellence in Molecular Cell Science, Shanghai, China.
D LiShanghai Information Center for Life Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
H-W ZhangDepartment of General Surgery, Zhongshan Hospital Affiliated to Fudan University, Shanghai, China.
M-F LiuCenter for RNA Research, State Key Laboratory of Molecular Biology-University of Chinese Academy of Sciences, CAS Center for Excellence in Molecular Cell Science, Shanghai, China.
Center for Excellence in Molecular Cell Science · CNChinese Academy of Sciences · CNShanghai Institutes for Biological Sciences · CNSun Yat-sen University · CNUniversity of Chinese Academy of Sciences · CNZhongshan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ErbB2 is a vital breast cancer gene and its overexpression has a decisive role in breast tumor initiation and malignant progression. However, the molecular mechanisms that underlie ErbB2 dysregulation in breast cancer cells remain incompletely understood. In this study, we found that ErbB2 expression is inversely correlated with the level of miR-155, a well-documented oncogenic miRNA, in ErbB2-positive breast tumors. We further determined that miR-155 potently suppresses ErbB2 in breast cancer cells. Mechanistically, miR-155 acts to downregulate ErbB2 via two distinct mechanisms. First, miR-155 represses ErbB2 transcription by targeting HDAC2, a transcriptional activator of ErbB2. Second, miR-155 directly targets ErbB2 via a regulatory element in its coding region. Intriguingly, miR-155 is upregulated by trastuzumab and in turn leads to a reduction of ErbB2 expression in trastuzumab-treated ErbB2-positive breast cancer cells. Functional studies showed that miR-155 inhibits ErbB2-induced malignant transformation of human breast epithelial cells. Thus, our findings reveal an intriguing miR-155-ErbB2 context in regulating the malignant transformation of breast epithelial cells, and thereby indicate a novel mode of action for miR-155 in ErbB2-positive breast cancer.

Indexed as

3' Untranslated RegionsAnimalsBreast NeoplasmsCell Line, TumorCell Transformation, NeoplasticDisease Models, AnimalEpithelial CellsErb-b2 Receptor Tyrosine KinasesFemaleGene Expression Regulation, NeoplasticHeterograftsHistone Deacetylase 2Histone DeacetylasesHumansMiceMicroRNAs3' Untranslated RegionsErb-b2 Receptor Tyrosine KinasesHDAC9 protein, humanHistone Deacetylase 2Histone DeacetylasesMicroRNAsMIRN155 microRNA, humanRepressor ProteinsRNA, MessengerTrastuzumab

Identifiers

PMID27065318
OpenAlexW2317017561

What OpenQuestion holds

Textmetadata
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.