Evidence map›Paper›PMID 26064277›Full record

ArticleInternational journal of clinical and experimental medicine2015

MiR-615 inhibited cell proliferation and cell cycle of human breast cancer cells by suppressing of AKT2 expression.

Yang Bai, Jingyan Li, Jie Li, Yonghong Liu, Bo Zhang

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.5field-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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
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  19. Frontiers in cellular and infection microbiology · 2018
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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 1 institution in 1 country.

Yang BaiDepartment of Surgical Oncology, Cangzhou Centerl Hospital Cangzhou, Hebei Province, P. R. China.
Jingyan LiDepartment of Radiology, Hebei province Cangzhou Hospital of integrated traditional and Western Medicine (Cangzhou NO. 2 Hospital) Cangzhou, Hebei Province, P. R. China.
Jie LiDepartment of Surgical Oncology, Cangzhou Centerl Hospital Cangzhou, Hebei Province, P. R. China.
Yonghong LiuDepartment of Surgical Oncology, Cangzhou Centerl Hospital Cangzhou, Hebei Province, P. R. China.
Bo ZhangDepartment of Surgical Oncology, Cangzhou Centerl Hospital Cangzhou, Hebei Province, P. R. China.
Cangzhou Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) have emerged as important regulators that potentially play critical roles in various biological processes. Previous studies have shown that miR-615 regulates proliferation and apoptosis in many types of cancers. The biological function of this microRNA in breast cancer remains largely unexplored. In the present study, we found that miR-615 expression was markedly downregulated in breast cancer tissues and breast cancer cells. The enforced expression of miR-615 was able to inhibite the proliferation and anchorage-independent growth of breast cancer cells, while miR-615-in showed the opposite effect. Bioinformatics analysis further revealed AKT2, a putative tumor promoter as a potential target of miR-615. Ectopic expression of miR-615 led to downregulation of AKT2 protein, which resulted in the upregulation of p27 and p21 and the downregulation of cyclin D1. In sum, these results suggest that miR-615 represents a potential anti-onco-miR and participates in breast cancer carcinogenesis by suppressing AKT2 expression.

Indexed as

AKT2breast cancercell cyclecell proliferationmiR-615

Identifiers

PMID26064277
PMCPMC4443111
OpenAlexW2203908836

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.