Evidence map›Paper›PMID 29561704›Full record

ArticleCancer biology & therapy2018

MiR-144 suppresses proliferation, invasion, and migration of breast cancer cells through inhibiting CEP55.

Yuanqin Yin, Jingjing Cai, Fandong Meng, Chengguang Sui, Youhong Jiang

Open access · bronzeAbstract read
In one paragraph

Article in Cancer biology & therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

36 citing papers in PubMed, 70 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. CEP55: Implications for Immunotherapy and Survival in Hepatocellular Carcinoma.Combinatorial chemistry & high throughput screening · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  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

5 authors at 2 institutions in 1 country.

Yuanqin Yina Biotherapy Laboratory, Cancer Institute , the First Affiliated Hospital of China Medical University , Shenyang , Liaoning , China.
Jingjing Caib Department of Medicine , General Hospital of Fushun Mining Bureau , Fushun , Liaoning , China.
Fandong Menga Biotherapy Laboratory, Cancer Institute , the First Affiliated Hospital of China Medical University , Shenyang , Liaoning , China.
Chengguang Suia Biotherapy Laboratory, Cancer Institute , the First Affiliated Hospital of China Medical University , Shenyang , Liaoning , China.
Youhong Jianga Biotherapy Laboratory, Cancer Institute , the First Affiliated Hospital of China Medical University , Shenyang , Liaoning , China.
China Medical University · CNFirst Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThe study aimed to investigate the molecular mechanism of miR-144 and CEP55 as well as the influence of their interaction on the cell proliferation, migration, invasion, cell cycle and cell apoptosis in breast cancer.

methodsIn this study, The Cancer Genome Atlas (TCGA, https://tcga-data.nci.nih.gov/ ) database was used for microarray analysis. The expressions of miR-144 and CEP55 in 40 adjacent tissues and 36 tumor tissues were examined by western blot, qRT-PCR and immunohistochemistry. The target relationship between miR-144 and CEP55 was predicted and confirmed by TargetScan and luciferase reporter assay. The cell proliferation, cell cycle and cell apoptosis in different groups were detected by MTT and flow cytometry assays, while wound healing and transwell assays were used for the cell migration and invasion tests. The regulatory effects of miR-144 and CEP55 on breast tumor were verified through nude mouse model in vivo experiment.

resultsMiR-144 was down-regulated in breast cancerous tissues and cells, whereas CEP55 expression was up-regulated in breast cancerous tissues. Moreover, there existed a target relationship between miR-144 and CEP55 and negative correlation on their expressions. MiR-144 could down-regulate CEP55 expression, thereby inhibiting proliferation, invasion, migration, retarding cell cycle and accelerating cell apoptosis. MiR-144 could inhibit cell progression through down-regulating CEP55 in vivo.

conclusionMiR-144 suppressed cell proliferation, migration, invasion and induced cell cycle arrest and cell apoptosis by repressing CEP55. This might provide a promising therapy for clinical treatment.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsApoptosisBreastBreast NeoplasmsCell Cycle CheckpointsCell Cycle ProteinsCell Line, TumorCell MovementCell ProliferationDown-RegulationFemaleHEK293 CellsHumansMiceMice, Inbred BALB CCell Cycle ProteinsCep55 protein, humanMicroRNAsMIRN144 microRNA, humanNuclear ProteinsBreast cancerCEP55miR-144Nude mouse model

Identifiers

PMID29561704
PMCPMC5902245
OpenAlexW2792579465

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.