Evidence map›Paper›PMID 26020378›Full record

ArticleMedicine2015

Downregulated miR-495 [Corrected] Inhibits the G1-S Phase Transition by Targeting Bmi-1 in Breast Cancer.

Lan Wang, Jun-Ling Liu, Liang Yu, Xiang-Xia Liu, Hong-Mei Wu, Fang-Yong Lei, Shu Wu, Xi Wang

Erratum issuedOpen access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

18 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. MicroRNA Regulation of Breast Cancer Stemness.International journal of molecular sciences · 2021
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Regulation of epithelial-mesenchymal transition through microRNAs: clinical and biological significance of microRNAs in breast cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
  17. Review
  18. Review
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

8 authors at 2 institutions in 4 countries.

Lan WangFrom the Department of Pathogen Biology and Immunology, School of Basic Courses, Guangdong Pharmaceutical University (LW, H-MW); Department of Medical Oncology, Sun Yat-sen University Cancer Center (JLL); Department of Vascular and Breast Surgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou (LY); Department of Plastic Surgery, the First Affiliated Hospital of Sun Yat-sen University (X-XL); State Key Laboratory of Oncology in South China (F-YL, SW); State Key Laboratory of Oncology in Southern China, Department of Experimental Research, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, China (XW).
Jun-Ling Liu
Liang Yu
Xiang-Xia Liu
Hong-Mei Wu
Fang-Yong Lei
Shu Wu
Xi Wang
X-Fab (Germany) · DESun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bmi-1 (B cell-specific Moloney murine leukemia virus integration site 1) is upregulated in breast cancer and was involved in many malignant progressions of breast cells, including cell proliferation, stem cell pluripotency, and cancer initiation. However, the epigenetic regulatory mechanism of Bmi-1 in breast cancer remains unclear. After analysis of the ArrayExpress dataset GSE45666, we comparatively detected the expression levels of miR-495 in 9 examined breast cancer cell lines, normal breast epithelial cells and 8 pairs of fresh clinical tumor samples. Furthermore, to evaluate the effect of miR-495 on the progression of breast cancer, MCF-7 and MDA-MB-231 were transduced to stably overexpress miR-495. The 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay, colony formation assays, 5-Bromo-2-deoxyUridine labeling and immunofluorescence, anchorage-independent growth ability assay, flow cytometry analysis, and luciferase assays were used to test the effect of miR-495 in MCF-7 and MDA-MB-231 cells in vitro. Xenografted tumor model was also used to evaluate the effect of miR-495 in breast cancer. Herein, we found that miR-495, a predicted regulator of Bmi-1, was frequently downregulated in malignant cells and tissues of breast. Upregulation of miR-495 significantly suppressed breast cancer cell proliferation and tumorigenicity via G1-S arrest. Further analysis revealed that miR-495 targeted Bmi-1 through its 3' untranslated region. Moreover, Bmi-1 could neutralize the suppressive effect of miR-495 on cell proliferation and tumorigenicity of breast cancer in vivo. These data suggested that miR-495 could inhibit the G1-S phase transition that leads to proliferation and tumorigenicity inhibition by targeting and suppressing Bmi-1 in breast cancer.

Indexed as

3' Untranslated RegionsAnimalsBlotting, WesternBreast NeoplasmsCell Line, TumorCell ProliferationDisease Models, AnimalDown-RegulationFemaleHumansMCF-7 CellsMiceMicroRNAsPhase TransitionPolycomb Repressive Complex 1Proto-Oncogene Proteins3' Untranslated RegionsBmi1 protein, mouseMicroRNAsMIRN495 microRNA, humanMIRN495 microRNA, mousePolycomb Repressive Complex 1Proto-Oncogene Proteins

Identifiers

PMID26020378
PMCPMC4616407
OpenAlexW2277241599

What OpenQuestion holds

Textmetadata
LicenceCC BY-ND
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.